151 results match your criteria Genetic and Inflammatory Mechanisms in Stroke


Cellular Mechanisms of Human Atherogenesis: Focus on Chronification of Inflammation and Mitochondrial Mutations.

Front Pharmacol 2020 14;11:642. Epub 2020 May 14.

Laboratory of Infection Pathology and Molecular Microecology, Institute of Human Morphology, Moscow, Russia.

Atherosclerosis is one of the most common diseases of the cardiovascular system that leads to the development of life-threatening conditions, such as heart attack and stroke. Arthrosclerosis affects various arteries in the human body, but is especially dangerous in the arteries alimenting heart and brain, aorta, and arteries of the lower limbs. By its pathophysiology, atherosclerosis is an inflammatory disease. Read More

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http://dx.doi.org/10.3389/fphar.2020.00642DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7247837PMC

Biophysical basis for Kv1.3 regulation of membrane potential changes induced by P2X4-mediated calcium entry in microglia.

Glia 2020 Jun 11. Epub 2020 Jun 11.

Department of Pharmacology, University of California, Davis, California, USA.

Microglia-mediated inflammation exerts adverse effects in ischemic stroke and in neurodegenerative disorders such as Alzheimer's disease (AD). Expression of the voltage-gated potassium channel Kv1.3 is required for microglia activation. Read More

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http://dx.doi.org/10.1002/glia.23847DOI Listing

Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies.

Int J Mol Sci 2020 May 29;21(11). Epub 2020 May 29.

Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research Raebareli (NIPER-R), Near CRPF Base Camp, Post Office Mati, Sarojini Nagar, Lucknow (U.P.) 226002, India.

Heavy metals are considered a continuous threat to humanity, as they cannot be eradicated. Prolonged exposure to heavy metals/metalloids in humans has been associated with several health risks, including neurodegeneration, vascular dysfunction, metabolic disorders, cancer, etc. Small blood vessels are highly vulnerable to heavy metals as they are directly exposed to the blood circulatory system, which has comparatively higher concentration of heavy metals than other organs. Read More

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http://dx.doi.org/10.3390/ijms21113862DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7313017PMC

Activated αβ on platelets mediates flow-dependent NETosis via SLC44A2.

Elife 2020 Apr 21;9. Epub 2020 Apr 21.

Centre for Haematology, Department of Immunology and Inflammation, Imperial College London, London, United Kingdom.

Platelet-neutrophil interactions are important for innate immunity, but also contribute to the pathogenesis of deep vein thrombosis, myocardial infarction and stroke. Here we report that, under flow, von Willebrand factor/glycoprotein Ibα-dependent platelet 'priming' induces integrin αβ activation that, in turn, mediates neutrophil and T-cell binding. Binding of platelet αβ to SLC44A2 on neutrophils leads to mechanosensitive-dependent production of highly prothrombotic neutrophil extracellular traps. Read More

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http://dx.doi.org/10.7554/eLife.53353DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253179PMC

Cerebral ischemia-reperfusion aggravated cerebral infarction injury and possible differential genes identified by RNA-Seq in rats.

Brain Res Bull 2020 Mar 23;156:33-42. Epub 2019 Dec 23.

State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China; Beijing Key Laboratory of Drug Target Identification and New Drug Sreeening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China. Electronic address:

Numerous studies have shown that local excessive inflammatory response in brain tissue was an important pathogenesis of secondary injury following cerebral ischemia-reperfusion (I/R). However, the inflammatory-related targets and pathways after cerebral I/R injury are still unclear. This study was to investigate possible targets and mechanisms after cerebral I/R injury. Read More

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http://dx.doi.org/10.1016/j.brainresbull.2019.12.014DOI Listing

Statins: Complex outcomes but increasingly helpful treatment options for patients.

Eur J Pharmacol 2019 Nov 27;863:172704. Epub 2019 Sep 27.

Cancer & Complex Systems Research Group, Medical Faculty, Westfaelian Wilhelms University of Muenster, Muenster, Germany. Electronic address:

Statins are long known class of medicines and the most frequently prescribed drugs in cardiovascular pharmacotherapy, widely ordered not only in patients suffering from dyslipidemia, but also in patients with coronary artery disease, acute coronary syndromes, diabetes mellitus, stroke, hypertension, and chronic kidney disease, with or without coexisting dyslipidemia. However, several clinical trials have shown, that the advantages of statins goes beyond their reduction of the cholesterol level. Some crucial isoprenoid mediators which are highly essential for the activation of different intracellular/signaling proteins, that play important roles in multiple cellular mechanisms, are regulated by statins in addition to the inhibition of cholesterol biosynthesis. Read More

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http://dx.doi.org/10.1016/j.ejphar.2019.172704DOI Listing
November 2019
2 Reads

Metabolic and Vascular Effect of the Mediterranean Diet.

Int J Mol Sci 2019 Sep 23;20(19). Epub 2019 Sep 23.

U.O.C di Medicina Interna con Stroke Care, Dipartimento di Promozione della Salute, Materno Infantile, Medicina Interna e Specialistica di Eccellenza "G. D'Alessandro" (PROMISE), University of Palermo, Piazza delle Cliniche n.2, 90127 Palermo, Italy.

Several studies indicated how dietary patterns that were obtained from nutritional cluster analysis can predict disease risk or mortality. Low-grade chronic inflammation represents a background pathogenetic mechanism linking metabolic risk factors to increased risk of chronic degenerative diseases. A Mediterranean diet (MeDi) style has been reported as associated with a lower degree of inflammation biomarkers and with a protective role on cardiovascular and cerebrovascular events. Read More

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http://dx.doi.org/10.3390/ijms20194716DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6801699PMC
September 2019
1 Read

Role of flavonoids in thrombotic, cardiovascular, and inflammatory diseases.

Inflammopharmacology 2019 Oct 15;27(5):863-869. Epub 2019 Jul 15.

Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, United Arab Emirates.

The failure of mechanisms of natural anti-coagulation either due to genetic impairment or due to severe external injuries may result in a condition called thrombosis. This is believed to be the primary cause for a variety of life-threatening conditions such as: heart attack, stroke, pulmonary embolism, thrombophlebitis, and deep venous thrombosis (DVT). The growing number of these incidents requires an alternative anti-coagulant or anti-thrombotic agent that has minimal side effects and improved efficiency. Read More

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http://dx.doi.org/10.1007/s10787-019-00612-6DOI Listing
October 2019
2 Reads

Absence of MCP-induced Protein 1 Enhances Blood-Brain Barrier Breakdown after Experimental Stroke in Mice.

Int J Mol Sci 2019 Jun 30;20(13). Epub 2019 Jun 30.

Burnett School of Biomedical Sciences, University of Central Florida College of Medicine, 4000 Central Florida Blvd, Orlando, FL 32816, USA.

Focal cerebral ischemia can cause blood-brain barrier (BBB) breakdown, which is implicated in neuroinflammation and progression of brain damage. Monocyte chemotactic protein 1-induced protein 1 (MCPIP1) is a newly identified zinc-finger protein that negatively regulates inflammatory signaling pathways. We aimed to evaluate the impact of genetic MCPIP1 deletion on BBB breakdown and expression of BBB-related matrix metalloproteinases (MMPs) and tight junction proteins after cerebral ischemia/reperfusion (I/R) using MCPIP1-deficient (MCPIP1) mice. Read More

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http://dx.doi.org/10.3390/ijms20133214DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6651107PMC
June 2019
2 Reads

Trim47 is a critical regulator of cerebral ischemia-reperfusion injury through regulating apoptosis and inflammation.

Biochem Biophys Res Commun 2019 08 6;515(4):651-657. Epub 2019 Jun 6.

Department of Geriatrics, The Affiliated Hospital of Shaanxi University Chinese Medicine, Xianyang, Shaanxi, 712000, China. Electronic address:

Cerebral ischemia is a leading cause of death and long-term disability in the world. Tripartite motif-47 (Trim47), a member of the TRIM family proteins, has been reported to be involved in apoptosis and inflammation in various types of diseases. Nevertheless, the underlying molecular mechanism of Trim47 in cerebral ischemia/reperfusion (I/R) injury remains unclear. Read More

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http://dx.doi.org/10.1016/j.bbrc.2019.05.065DOI Listing
August 2019
3 Reads

Targeting RIPK1 for the treatment of human diseases.

Proc Natl Acad Sci U S A 2019 05 2;116(20):9714-9722. Epub 2019 May 2.

Department of Cell Biology, Harvard Medical School, Boston, MA 02115

RIPK1 kinase has emerged as a promising therapeutic target for the treatment of a wide range of human neurodegenerative, autoimmune, and inflammatory diseases. This was supported by extensive studies which demonstrated that RIPK1 is a key mediator of apoptotic and necrotic cell death as well as inflammatory pathways. Furthermore, human genetic evidence has linked the dysregulation of RIPK1 to the pathogenesis of ALS as well as other inflammatory and neurodegenerative diseases. Read More

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http://dx.doi.org/10.1073/pnas.1901179116DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6525537PMC
May 2019
3 Reads

Effect of Inflammation on the Process of Stroke Rehabilitation and Poststroke Depression.

Front Psychiatry 2019 11;10:184. Epub 2019 Apr 11.

Department of General Surgery, Second Hospital of Jilin University, Changchun, China.

A considerable body of evidence has shown that inflammation plays an important role in the process of stroke rehabilitation and development of poststroke depression (PSD). However, the specific molecular and cellular mechanisms involved remain unclear. In this review, we summarize how neuroinflammation affects stroke rehabilitation and PSD. Read More

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http://dx.doi.org/10.3389/fpsyt.2019.00184DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6470379PMC
April 2019
5 Reads

TRPV4 is a regulator in P. gingivalis lipopolysaccharide-induced exacerbation of macrophage foam cell formation.

Physiol Rep 2019 04;7(7):e14069

Department of Nutrition and Food Science, University of Maryland, College Park, Maryland.

Porphyromonas gingivalis (P.g), a major causative agent of periodontitis, has been linked to atherosclerosis, a chronic inflammatory vascular disease. Recent studies have suggested a link between periodontitis and arterial stiffness, a risk factor for atherosclerosis. Read More

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https://onlinelibrary.wiley.com/doi/abs/10.14814/phy2.14069
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http://dx.doi.org/10.14814/phy2.14069DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6461712PMC
April 2019
7 Reads

Shared genetic risk factors for depression and stroke.

Prog Neuropsychopharmacol Biol Psychiatry 2019 07 18;93:55-70. Epub 2019 Mar 18.

Department of Psychosomatics and Psychiatry, ZhongDa Hospital, School of Medical, Institute of Psychosomatics, Southeast University, China. Electronic address:

Background: The comorbidity of major depressive disorder (MDD) and stroke are common in clinic. There is a growing body of evidence suggesting a bi-directional relationship between stroke and depression. However, the mechanisms underlying the relationship between MDD and stroke are poorly investigated. Read More

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http://dx.doi.org/10.1016/j.pnpbp.2019.03.003DOI Listing
July 2019
18 Reads

β-Arrestin-2-ERK1/2 cPLAα axis mediates TLR4 signaling to influence eicosanoid induction in ischemic brain.

FASEB J 2019 05 22;33(5):6584-6595. Epub 2019 Feb 22.

Department of Emergency Medicine and Chest Pain Center, Qilu Hospital of Shandong University, Jinan, China.

LPS has been shown to elicit neuroinflammation associated with the up-regulation of the eicosanoid pathway in animal models; however, the regulatory mechanisms of TLR4 in brain neuroinflammatory conditions remain elusive. β-Arrestins are key regulators of the GPCR signaling pathway and are involved in the leukotriene B4-induced leukocyte migration to initiate inflammatory response. However, the roles of β-arrestins in eicosanoid regulation and related diseases are not clear. Read More

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http://dx.doi.org/10.1096/fj.201802020RDOI Listing
May 2019
4 Reads

How Might Bromodomain and Extra-Terminal (BET) Inhibitors Operate in Cardiovascular Disease?

Am J Cardiovasc Drugs 2019 Apr;19(2):107-111

School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong SAR, China.

Bromodomain and extra-terminal (BET) inhibitors, acting via epigenetic mechanisms, have been developed recently as potential new treatments for cancer, including prostate cancer, and inflammatory conditions. Some BET inhibitors, such as RVX-208, also raise high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-1 levels. A recent meta-analysis of three small trials (n = 798) found that RVX-208 protected against major adverse cardiovascular events (MACE), raising the question as to whether this protective effect was an artefact, a chance finding, or mediated by HDL-C, anti-inflammatory pathways, or other factors. Read More

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http://dx.doi.org/10.1007/s40256-018-00315-3DOI Listing
April 2019
3 Reads

Neutrophil elastase plays a non-redundant role in remodeling the venular basement membrane and neutrophil diapedesis post-ischemia/reperfusion injury.

J Pathol 2019 05 22;248(1):88-102. Epub 2019 Mar 22.

William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.

Ischemia/reperfusion (I/R) injury is a severe inflammatory insult associated with numerous pathologies, such as myocardial infarction, stroke and acute kidney injury. I/R injury is characterized by a rapid influx of activated neutrophils secreting toxic free radical species and degrading enzymes that can irreversibly damage the tissue, thus impairing organ functions. Significant efforts have been invested in identifying therapeutic targets to suppress neutrophil recruitment and activation post-I/R injury. Read More

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http://dx.doi.org/10.1002/path.5234DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850085PMC
May 2019
17 Reads

Endocrine Regulator rFGF21 (Recombinant Human Fibroblast Growth Factor 21) Improves Neurological Outcomes Following Focal Ischemic Stroke of Type 2 Diabetes Mellitus Male Mice.

Stroke 2018 12;49(12):3039-3049

Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston (Y.J., N.L., Q.W., Z.Y., L.L., J.Y., S.G., B.J.A., E.H.L., X.W.).

Background and Purpose- The complexity and heterogeneity of stroke, as well as the associated comorbidities, may render neuroprotective drugs less efficacious in clinical practice. Therefore, the development of targeted therapies to specific patient subsets has become a high priority in translational stroke research. Ischemic stroke with type 2 diabetes mellitus has a nearly double mortality rate and worse neurological outcomes. Read More

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http://dx.doi.org/10.1161/STROKEAHA.118.022119DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6310061PMC
December 2018
67 Reads

Genetic Susceptibility Loci for Cardiovascular Disease and Their Impact on Atherosclerotic Plaques.

Circ Genom Precis Med 2018 09;11(9):e002115

Laboratory of Experimental Cardiology, Division Heart and Lungs, University Medical Center Utrecht, University Utrecht, The Netherlands (S.W.v.d.L., M.A.S., S.H., H.M.d.R., G.P.).

Background: Atherosclerosis is a chronic inflammatory disease in part caused by lipid uptake in the vascular wall, but the exact underlying mechanisms leading to acute myocardial infarction and stroke remain poorly understood. Large consortia identified genetic susceptibility loci that associate with large artery ischemic stroke and coronary artery disease. However, deciphering their underlying mechanisms are challenging. Read More

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https://www.ahajournals.org/doi/10.1161/CIRCGEN.118.002115
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http://dx.doi.org/10.1161/CIRCGEN.118.002115DOI Listing
September 2018
52 Reads

Genetic Deletion of PGF-FP Receptor Exacerbates Brain Injury Following Experimental Intracerebral Hemorrhage.

Front Neurosci 2018 5;12:556. Epub 2018 Sep 5.

Department of Anesthesiology, University of Florida, College of Medicine, Gainesville, FL, United States.

The release of inflammatory molecules such as prostaglandins (e.g., PGF) is associated with brain damage following an intracerebral hemorrhagic (ICH) stroke; however, the role of PGF and its cognate FP receptor in ICH remains unclear. Read More

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http://dx.doi.org/10.3389/fnins.2018.00556DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6134069PMC
September 2018
9 Reads

Genome-Wide Expression Profiles for Ischemic Stroke: A Meta-Analysis.

J Stroke Cerebrovasc Dis 2018 Nov 28;27(11):3336-3341. Epub 2018 Aug 28.

Laboratory of Neuropsychiatric Genetics, Biomedical Sciences Research Group, School of Medicine, Universidad Antonio Nariño, Bogotá, Colombia. Electronic address:

Background: Genome-wide expression studies (GWES), using microarray platforms, have allowed a deeper understanding of the molecular factors involved in the pathophysiology of ischemic stroke (IS), one of the main global causes of mortality and disability.

Methods: In the current work, we carried out a meta-analysis of available GWES for IS. Bioinformatics and computational biology analyses were applied to identify enriched functional categories and convergence with other genomic datasets for IS. Read More

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http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2018.07.035DOI Listing
November 2018
35 Reads

Associations of Asthma and Asthma Control With Atrial Fibrillation Risk: Results From the Nord-Trøndelag Health Study (HUNT).

JAMA Cardiol 2018 08;3(8):721-728

Department of Public Health and Nursing, Faculty of Medicine and Health Science, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.

Importance: Asthma, a chronic inflammatory airway disease, and atrial fibrillation (AF) share several common pathophysiological mechanisms. Research on the association between asthma and atrial fibrillation is lacking, and to our knowledge, no previous studies have assessed the dose-response association between levels of asthma control and AF.

Objective: To assess the association between asthma, levels of asthma control, and AF. Read More

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http://dx.doi.org/10.1001/jamacardio.2018.1901DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6143075PMC
August 2018
17 Reads

Targeting vascular inflammation in ischemic stroke: Recent developments on novel immunomodulatory approaches.

Eur J Pharmacol 2018 Aug 20;833:531-544. Epub 2018 Jun 20.

Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS, USA. Electronic address:

Ischemic stroke is a devastating and debilitating medical condition with limited therapeutic options. However, accumulating evidence indicates a central role of inflammation in all aspects of stroke including its initiation, the progression of injury, and recovery or wound healing. A central target of inflammation is disruption of the blood brain barrier or neurovascular unit. Read More

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http://dx.doi.org/10.1016/j.ejphar.2018.06.028DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090562PMC
August 2018
8 Reads

Neuroimmune disorders of the central nervous system in children in the molecular era.

Nat Rev Neurol 2018 07;14(7):433-445

Department of Neurology and Pediatric Multiple Sclerosis Clinic, Children's Hospital of Philadelphia, Philadelphia, PA, USA.

Immune-mediated disorders of the CNS in children are a complex group of demyelinating, inflammatory, parainfectious and postinfectious disorders with heterogeneous pathobiological mechanisms and clinical manifestations, often associated with fundamental derangement in immune regulation. In this Review, we aim to provide an update on our knowledge of neuroimmune disorders and highlight areas of research that are priorities for improving clinical management. We outline the clinical features of neuroimmune disorders, the current approaches to their treatment and new approaches in development. Read More

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http://dx.doi.org/10.1038/s41582-018-0024-9DOI Listing
July 2018
26 Reads

Migraine and cerebrovascular disease: still a dangerous connection?

Neurol Sci 2018 Jun;39(Suppl 1):33-37

Neurology and Stroke Unit, Department of Neurosciences, Niguarda Ca' Granda Hospital, Piazza Ospedale Maggiore, 3, 20162, Milan, Italy.

Migraine is a common type of headache in young adults, with an estimated prevalence of 4% before puberty and as high as 25% in women by their mid to late 30s. About one third of migraineurs experience transient neurological symptoms known as auras, which characterize a variant known as migraine with aura. Many evidences have shown an increased risk of vascular events in patients affected by migraine, particularly among women and among migraine patients with aura. Read More

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http://dx.doi.org/10.1007/s10072-018-3429-8DOI Listing
June 2018
7 Reads

Psoriasis as a cardiovascular risk factor: updates and algorithmic approach.

G Ital Dermatol Venereol 2018 Oct 19;153(5):659-665. Epub 2018 Apr 19.

Department of Dermatology, San Martino Policlinic, University of Genoa, Genoa, Italy.

Although psoriasis is predominantly a chronic inflammatory skin disorder, it has been known to be associated with cardiovascular disease. Patients with psoriasis, particularly with moderate to severe forms, present an increased rate of cardiovascular mortality, myocardial infarction and stroke. However the pathophysiology of the relationship between psoriasis and cardiovascular risk and comorbidities has not yet completely known. Read More

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http://dx.doi.org/10.23736/S0392-0488.18.06040-6DOI Listing
October 2018
6 Reads

Epicardial adipose tissue and atrial fibrillation: pathophysiological mechanisms, clinical implications, and potential therapies.

Curr Med Res Opin 2018 11 3;34(11):1933-1943. Epub 2018 May 3.

c Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Department of Cardiology , Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University , Tianjin , PR China.

Background: Atrial fibrillation (AF) is the most common arrhythmia in clinical practice and is associated with increased cardiovascular morbidity and mortality. Epicardial adipose tissue (EAT) serves as a biologically active organ with important endocrine and inflammatory function. Review An accumulating body of evidence suggests that EAT is associated with the initiation, perpetuation, and recurrence of AF, but the precise role of EAT in AF pathogenesis is not completely elucidated. Read More

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http://dx.doi.org/10.1080/03007995.2018.1462786DOI Listing
November 2018
7 Reads

Neurological syndromes driven by postinfectious processes or unrecognized persistent infections.

Curr Opin Neurol 2018 06;31(3):318-324

Section of Infections of the Nervous System, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA.

Purpose Of Review: The immune system serves a critical role in protecting the host against various pathogens. However, under circumstances, once triggered by the infectious process, it may be detrimental to the host. This may be as a result of nonspecific immune activation or due to a targeted immune response to a specific host antigen. Read More

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http://dx.doi.org/10.1097/WCO.0000000000000553DOI Listing
June 2018
5 Reads

Thioredoxin-Interacting Protein (TXNIP) in Cerebrovascular and Neurodegenerative Diseases: Regulation and Implication.

Mol Neurobiol 2018 Oct 27;55(10):7900-7920. Epub 2018 Feb 27.

Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, Wittenborg Bldg, Room-231, Memphis, TN, 38163, USA.

Neurological diseases, including acute attacks (e.g., ischemic stroke) and chronic neurodegenerative diseases (e. Read More

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http://link.springer.com/10.1007/s12035-018-0917-z
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http://dx.doi.org/10.1007/s12035-018-0917-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6388721PMC
October 2018
9 Reads

Hypoxia Triggers SENP1 (Sentrin-Specific Protease 1) Modulation of KLF15 (Kruppel-Like Factor 15) and Transcriptional Regulation of Arg2 (Arginase 2) in Pulmonary Endothelium.

Arterioscler Thromb Vasc Biol 2018 04 22;38(4):913-926. Epub 2018 Feb 22.

From the Departments of Anesthesiology and Critical Care Medicine (D.P., Y.N., M.C.R., D.H., A.B., L.S., D.B., L.R.), Cell Biology (L.R.), Biomedical Engineering (D.B., L.R.), and Pediatrics, and the Center for Cell Dynamics (L.R.), Division of Cardiology (G.K., T.L.), and Division of Pulmonary and Critical Care Medicine, Department of Medicine (L.A.S.), Johns Hopkins Medical Institutions, Baltimore, MD.

Objective: KLF15 (Kruppel-like factor 15) has recently been shown to suppress activation of proinflammatory processes that contribute to atherogenesis in vascular smooth muscle, however, the role of KLF15 in vascular endothelial function is unknown. Arginase mediates inflammatory vasculopathy and vascular injury in pulmonary hypertension. Here, we tested the hypothesis that KLF15 is a critical regulator of hypoxia-induced Arg2 (arginase 2) transcription in human pulmonary microvascular endothelial cells (HPMEC). Read More

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http://dx.doi.org/10.1161/ATVBAHA.117.310660DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6738933PMC
April 2018
5 Reads

Atherothrombosis and Thromboembolism: Position Paper from the Second Maastricht Consensus Conference on Thrombosis.

Thromb Haemost 2018 02 29;118(2):229-250. Epub 2018 Jan 29.

Laboratory for Clinical Thrombosis and Haemostasis, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center, Maastricht, The Netherlands.

Atherothrombosis is a leading cause of cardiovascular mortality and long-term morbidity. Platelets and coagulation proteases, interacting with circulating cells and in different vascular beds, modify several complex pathologies including atherosclerosis. In the second Maastricht Consensus Conference on Thrombosis, this theme was addressed by diverse scientists from bench to bedside. Read More

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http://dx.doi.org/10.1160/TH17-07-0492DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6193488PMC
February 2018
17 Reads

Discovery of Leonuri and therapeutical applications: From bench to bedside.

Pharmacol Ther 2018 08 9;188:26-35. Epub 2018 Mar 9.

Shanghai Key Laboratory of Bioactive Small Molecules, Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201203, China. Electronic address:

Despite several advances in percutaneous coronary intervention and the discovery of new drugs, the incidence of myocardial infarction and deaths due to cardiovascular diseases (CVD) has not decreased markedly in China. The quality of life is affected seriously, which further results in great social and family burden. Many drugs, from the century-old aspirin to the newly FDA-approved Byvalson, have been proven to be effective in the treatment and prevention of CVD. Read More

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http://dx.doi.org/10.1016/j.pharmthera.2018.01.006DOI Listing
August 2018
12 Reads

C-Phycocyanin and Phycocyanobilin as Remyelination Therapies for Enhancing Recovery in Multiple Sclerosis and Ischemic Stroke: A Preclinical Perspective.

Behav Sci (Basel) 2018 Jan 18;8(1). Epub 2018 Jan 18.

Center for Genetic Engineering and Biotechnology (CIGB), Ave. 31 e/158 y 190, Cubanacan, P.O. Box 6162, Playa, Havana 10600, Cuba.

Myelin loss has a crucial impact on behavior disabilities associated to Multiple Sclerosis (MS) and Ischemic Stroke (IS). Although several MS therapies are approved, none of them promote remyelination in patients, limiting their ability for chronic recovery. With no available therapeutic options, enhanced demyelination in stroke survivors is correlated with a poorer behavioral recovery. Read More

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http://dx.doi.org/10.3390/bs8010015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5791033PMC
January 2018
25 Reads

IL-23 (Interleukin-23)-Producing Conventional Dendritic Cells Control the Detrimental IL-17 (Interleukin-17) Response in Stroke.

Stroke 2018 01 6;49(1):155-164. Epub 2017 Dec 6.

From the Department of Neurology (M. Gelderblom, P.L., V.T., P.A., B.R., C.G., T.M.), Institute of Neuropathology (C.B., M. Glatzel), Department for Neuroradiological Diagnosis and Intervention (J.S.), and Institute of Immunology (E.T.), University Medical Center Hamburg-Eppendorf, Germany; Department d'Isquèmia Cerebral i Neurodegeneració, Institut d'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas, Spain (M. Gallizioli, A.M.P.); Department of Neurology, Technical University of Munich, Germany (T.K.); Munich Cluster for Systems Neurology (SyNergy), Germany (T.K.); and Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore (T.V.A.).

Background And Purpose: Inflammatory mechanisms can exacerbate ischemic tissue damage and worsen clinical outcome in patients with stroke. Both αβ and γδ T cells are established mediators of tissue damage in stroke, and the role of dendritic cells (DCs) in inducing the early events of T cell activation and differentiation in stroke is not well understood.

Methods: In a murine model of experimental stroke, we defined the immune phenotype of infiltrating DC subsets based on flow cytometry of surface markers, the expression of ontogenetic markers, and cytokine levels. Read More

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http://dx.doi.org/10.1161/STROKEAHA.117.019101DOI Listing
January 2018
45 Reads

Neuronal CCL2 expression drives inflammatory monocyte infiltration into the brain during acute virus infection.

J Neuroinflammation 2017 Dec 4;14(1):238. Epub 2017 Dec 4.

Translational Neuroimmunology Lab, Mayo Clinic, Rochester, USA.

Background: Viral encephalitis is a dangerous compromise between the need to robustly clear pathogen from the brain and the need to protect neurons from bystander injury. Theiler's murine encephalomyelitis virus (TMEV) infection of C57Bl/6 mice is a model of viral encephalitis in which the compromise results in hippocampal damage and permanent neurological sequelae. We previously identified brain-infiltrating inflammatory monocytes as the primary driver of this hippocampal pathology, but the mechanisms involved in recruiting these cells to the brain were unclear. Read More

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http://dx.doi.org/10.1186/s12974-017-1015-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715496PMC
December 2017
13 Reads

RIP1K Contributes to Neuronal and Astrocytic Cell Death in Ischemic Stroke via Activating Autophagic-lysosomal Pathway.

Neuroscience 2018 02 8;371:60-74. Epub 2017 Nov 8.

Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu 215123, China; Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, School of Public Health, Soochow University, Suzhou 215123, China. Electronic address:

Although the receptor-interacting protein 1 kinase (RIP1K)-regulated necroptosis can be evoked by cerebral ischemia, the effects of RIP1K in mediating neuronal and astrocytic cell death and the underlying mechanisms remain poorly understood. This study evaluates the contribution of RIP1K to ischemic stroke-induced neuronal and astrocytic cell death, and the activation of autophagic-lysosomal pathway. Using an in vitro oxygen and glucose deprivation (OGD) in primary cultured neurons or astrocytes and a permanent middle cerebral artery occlusion (pMCAO) model in rats or mice, we observed the role of RIP1K in the ischemic neuronal and astrocytic cell death and the underlying mechanisms by pharmacological or genetic inhibition of RIP1K. Read More

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http://dx.doi.org/10.1016/j.neuroscience.2017.10.038DOI Listing
February 2018
26 Reads

Alcohol's Effects on the Cardiovascular System.

Authors:
Mariann R Piano

Alcohol Res 2017 ;38(2):219-241

Mariann R. Piano, Ph.D., is a Professor in and Department Head of the Department of Biobehavioral Health Science, University of Illinois at Chicago, Chicago, Illinois.

Alcohol use has complex effects on cardiovascular (CV) health. The associations between drinking and CV diseases such as hypertension, coronary heart disease, stroke, peripheral arterial disease, and cardiomyopathy have been studied extensively and are outlined in this review. Although many behavioral, genetic, and biologic variants influence the interconnection between alcohol use and CV disease, dose and pattern of alcohol consumption seem to modulate this most. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5513687PMC
May 2018
5 Reads

Association Between Clusterin Gene Polymorphisms and Epilepsy in a Han Chinese Population.

Genet Test Mol Biomarkers 2017 Nov 3;21(11):692-697. Epub 2017 Oct 3.

1 Department of Neurology, Nanfang Hospital, Southern Medical University , Guangzhou, Guangdong, China .

Background: Clusterin (CLU) is implicated in the inflammatory and apoptotic mechanisms of epilepsy, and the CLU gene has been associated with a number of other neurological diseases. In this study, we investigated the genetic association of CLU polymorphisms with epilepsy in a Han Chinese population.

Methods: A total of 249 epileptic patients and 289 healthy controls were included in this study. Read More

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http://www.liebertpub.com/doi/10.1089/gtmb.2017.0032
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http://dx.doi.org/10.1089/gtmb.2017.0032DOI Listing
November 2017
16 Reads

Venous thromboembolism: thrombosis, inflammation, and immunothrombosis for clinicians.

J Thromb Thrombolysis 2017 Oct;44(3):377-385

Instituto de Cardiología y Medicina Vascular, TecSalud and Centro de Investigacion Biomedica del Hospital Zambrano Hellion, Escuela de Medicina y Ciencias de la Salud, Tecnologico de Monterrey, San Pedro Garza Garcia, Nuevo Leon, Mexico.

Venous thromboembolism (VTE) is a worldwide disease related with mortality, cardiovascular disability, impaired quality of life and, cause major long-term complications. Clinicians related to the acute and long-term patients care must be involved in the molecular mechanisms of thrombosis. The vessel wall and its inner lining of the endothelium are critical to the maintenance of a patent vasculature. Read More

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http://link.springer.com/10.1007/s11239-017-1528-7
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http://dx.doi.org/10.1007/s11239-017-1528-7DOI Listing
October 2017
73 Reads

The Role of Emerging Risk Factors in Cardiovascular Outcomes.

Curr Atheroscler Rep 2017 Jun;19(6):28

Clinical Trial Service Unit and Epidemiological Studies Unit (CTSU), Nuffield Department of Population Health, University of Oxford, Richard Doll Building, Old Road Campus, Roosevelt Drive, Oxford, OX3 7LF, UK.

Purpose Of Review: This review discusses the recent evidence for a selection of blood-based emerging risk factors, with particular reference to their relation with coronary heart disease and stroke.

Recent Findings: For lipid-related emerging risk factors, recent findings indicate that increasing high-density lipoprotein cholesterol is unlikely to reduce cardiovascular risk, whereas reducing triglyceride-rich lipoproteins and lipoprotein(a) may be beneficial. For inflammatory and hemostatic biomarkers, genetic studies suggest that IL-6 (a pro-inflammatory cytokine) and several coagulation factors are causal for cardiovascular disease, but such studies do not support a causal role for C-reactive protein and fibrinogen. Read More

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http://dx.doi.org/10.1007/s11883-017-0661-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5419996PMC
June 2017
59 Reads

Inhibition of autophagy blocks cathepsins-tBid-mitochondrial apoptotic signaling pathway via stabilization of lysosomal membrane in ischemic astrocytes.

Cell Death Dis 2017 02 16;8(2):e2618. Epub 2017 Feb 16.

Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, College of Pharmaceutical Science; Department of Pharmacology and Laboratory of Cerebrovascular Pharmacology; Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, School of Public Health, Soochow University, Suzhou, China.

Our previous study and others have demonstrated that autophagy is activated in ischemic astrocytes and contributes to astrocytic cell death. However, the mechanisms of ischemia-induced autophagy remain largely unknown. In this study, we established a rat's model of permanent middle cerebral artery occlusion (pMCAO) and an in vitro oxygen and glucose deprivation (OGD) model. Read More

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http://dx.doi.org/10.1038/cddis.2017.34DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386481PMC
February 2017
34 Reads

Update about atrial fibrillation genetics.

Curr Opin Cardiol 2017 Feb 4. Epub 2017 Feb 4.

aCardiovascular Genetics Center, University of Girona - IDIBGI bCentro Investigación Biomédica en Red. Enfermedades Cardiovasculares (CIBERCV) cDepartment of Medical Sciences, School of Medicine, University of Girona dCardiomyopathies Unit, Hospital Josep Trueta, Girona, Spain.

Purpose Of Review: Atrial fibrillation is an important cause of morbidity in the aging population. The mechanisms responsible for the triggering and maintenance of the chaotic atrial rhythm are still poorly understood. In this review, we will focus on the genetic aspects of atrial fibrillation, to understand causality, with special emphasis on recent studies published in the field. Read More

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http://dx.doi.org/10.1097/HCO.0000000000000387DOI Listing
February 2017
33 Reads

Stroke Risk Factors, Genetics, and Prevention.

Circ Res 2017 Feb;120(3):472-495

From the Department of Epidemiology, Mailman School of Public Health (A.K.B., M.S.V.E.) and Department of Neurology, College of Physicians and Surgeons (A.K.B., C.E., M.S.V.E.), Columbia University, New York, NY.

Stroke is a heterogeneous syndrome, and determining risk factors and treatment depends on the specific pathogenesis of stroke. Risk factors for stroke can be categorized as modifiable and nonmodifiable. Age, sex, and race/ethnicity are nonmodifiable risk factors for both ischemic and hemorrhagic stroke, while hypertension, smoking, diet, and physical inactivity are among some of the more commonly reported modifiable risk factors. Read More

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https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.116.30839
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http://dx.doi.org/10.1161/CIRCRESAHA.116.308398DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5321635PMC
February 2017
16 Reads

Cannabinoid Type-2 Receptor Drives Neurogenesis and Improves Functional Outcome After Stroke.

Stroke 2017 01 29;48(1):204-212. Epub 2016 Nov 29.

From the Departamento de Farmacología, Facultad de Medicina, Instituto de Investigación Hospital 12 de Octubre (i+12) (I.B.-F., M.I.C., J.G.Z., J.M.P., O.H., V.G.R., I.L., M.A.M.), Departamento de Bioquímica y Biología Molecular I, Facultad de Ciencias Químicas, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS) and Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED) (J.D.-A., J.M.G.-S., M.G., I.G.-R.), and Instituto Universitario de Investigación en Neuroquímica (I.B.-F., M.I.C., J.M.P., O.H., J.D.-A., M.G., I.L., I.G.-R., M.A.M.), Universidad Complutense (UCM), Madrid, Spain.

Background And Purpose: Stroke is a leading cause of adult disability characterized by physical, cognitive, and emotional disturbances. Unfortunately, pharmacological options are scarce. The cannabinoid type-2 receptor (CB2R) is neuroprotective in acute experimental stroke by anti-inflammatory mechanisms. Read More

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http://dx.doi.org/10.1161/STROKEAHA.116.014793DOI Listing
January 2017
40 Reads

Electrical stimulation of cerebellar fastigial nucleus protects against cerebral ischemic injury by PPARγ upregulation.

Neurol Res 2017 Jan 7;39(1):23-29. Epub 2016 Nov 7.

b Department of Neurology , The Second Affiliated Hospital of Chongqing Medical University , Chongqing , China.

Objective: Cerebellar fastigial nucleus stimulation (FNS) has been shown to protect against cerebral ischemic injury. Peroxisome proliferator activator receptor gamma (PPARγ) has been reported to cause neuroprotection in animal models of stroke. The present study was performed to explore the neuroprotective mechanisms of FNS treatment in experimental stroke. Read More

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http://dx.doi.org/10.1080/01616412.2016.1251710DOI Listing
January 2017
116 Reads

Impact of Salt Intake on the Pathogenesis and Treatment of Hypertension.

Adv Exp Med Biol 2017 ;956:61-84

Institute of Environmental Health, Centre for Public Health, Medical University of Vienna, Kinderspitalgasse 15, 1090, Vienna, Austria.

Excessive dietary salt (sodium chloride) intake is associated with an increased risk for hypertension, which in turn is especially a major risk factor for stroke and other cardiovascular pathologies, but also kidney diseases. Besides, high salt intake or preference for salty food is discussed to be positive associated with stomach cancer, and according to recent studies probably also obesity risk. On the other hand a reduction of dietary salt intake leads to a considerable reduction in blood pressure, especially in hypertensive patients but to a lesser extent also in normotensives as several meta-analyses of interventional studies have shown. Read More

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http://dx.doi.org/10.1007/5584_2016_147DOI Listing
October 2017
44 Reads

Relationship between Interleukin-6 (-174G/C and -572C/G) Promoter Gene Polymorphisms and Risk of Intracerebral Hemorrhage: A Meta-Analysis.

Pulse (Basel) 2016 Sep 14;4(2-3):61-68. Epub 2016 Jul 14.

Department of Neurology, All India Institute of Medical Sciences, New Delhi, India.

Background: Polymorphisms of -174G/C and -572C/G in the Interleukin-6 (IL-6) promoter gene can affect both transcription and secretion of IL-6 and may be involved in the inflammatory mechanisms in early and delayed phases after intracerebral hemorrhage (ICH). The role of these polymorphisms remains unclear for the pathogenesis of ICH.

Methods: PubMed, EMBASE, MEDLINE and Google Scholar searches were conducted from January 1, 1950 to February 29, 2016 and were supplemented with relevant articles identified in the references. Read More

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http://dx.doi.org/10.1159/000447677DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5052694PMC
September 2016
23 Reads

Insights into the epigenetic mechanisms involving histone lysine methylation and demethylation in ischemia induced damage and repair has therapeutic implication.

Biochim Biophys Acta Mol Basis Dis 2017 01 21;1863(1):152-164. Epub 2016 Sep 21.

CSIR-Centre for Cellular and Molecular Biology (CCMB), Habsiguda, Uppal Road, Hyderabad 500007, India. Electronic address:

Cerebral ischemic stroke is one of the leading causes of death and disability worldwide. Therapeutic interventions to minimize ischemia-induced neural damage are limited due to poor understanding of molecular mechanisms mediating complex pathophysiology in stroke. Recently, epigenetic mechanisms mostly histone lysine (K) acetylation and deacetylation have been implicated in ischemic brain damage and have expanded the dimensions of potential therapeutic intervention to the systemic/local administration of histone deacetylase inhibitors. Read More

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http://dx.doi.org/10.1016/j.bbadis.2016.09.014DOI Listing
January 2017
22 Reads

Oxidative stress and inflammation in cerebral cavernous malformation disease pathogenesis: Two sides of the same coin.

Int J Biochem Cell Biol 2016 12 14;81(Pt B):254-270. Epub 2016 Sep 14.

University of Rochester Medical Center, School of Medicine and Dentistry, 601 Elmwood Ave, 14642 Rochester, NY, USA. Electronic address:

Cerebral Cavernous Malformation (CCM) is a vascular disease of proven genetic origin, which may arise sporadically or is inherited as an autosomal dominant condition with incomplete penetrance and highly variable expressivity. CCM lesions exhibit a range of different phenotypes, including wide inter-individual differences in lesion number, size, and susceptibility to intracerebral hemorrhage (ICH). Lesions may remain asymptomatic or result in pathological conditions of various type and severity at any age, with symptoms ranging from recurrent headaches to severe neurological deficits, seizures, and stroke. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S13572725163027
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http://dx.doi.org/10.1016/j.biocel.2016.09.011DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5155701PMC
December 2016
5 Reads

Apoptosis-Resistant Cardiac Progenitor Cells Modified With Apurinic/Apyrimidinic Endonuclease/Redox Factor 1 Gene Overexpression Regulate Cardiac Repair After Myocardial Infarction.

Stem Cells Transl Med 2016 Aug 22;5(8):1067-78. Epub 2016 Jun 22.

Department of Internal Medicine, Division of Cardiology, Nephrology, Pulmonology, and Neurology, Asahikawa Medical University, Asahikawa, Japan.

Unlabelled: : Overcoming the insufficient survival of cell grafts is an essential objective in cell-based therapy. Apurinic/apyrimidinic endonuclease/redox factor 1 (APE1) promotes cell survival and may enhance the therapeutic effect of engrafted cells. The aim of this study is to determine whether APE1 overexpression in cardiac progenitor cells (CPCs) could ameliorate the efficiency of cell-based therapy. Read More

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http://dx.doi.org/10.5966/sctm.2015-0281DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4954451PMC
August 2016
22 Reads