4,202 results match your criteria Basic research in cardiology[Journal]


Remote ischemic preconditioning reduces myocardial ischemia-reperfusion injury through unacylated ghrelin-induced activation of the JAK/STAT pathway.

Basic Res Cardiol 2020 Jun 30;115(4):50. Epub 2020 Jun 30.

Department of Anesthesiology, Sapporo Medical University School of Medicine, S-1, W-16, Chuo-ku, Sapporo, Hokkaido, 060-8543, Japan.

Remote ischemic preconditioning (RIPC) offers cardioprotection against myocardial ischemia-reperfusion injury. The humoral factors involved in RIPC that are released from parasympathetically innervated organs have not been identified. Previous studies showed that ghrelin, a hormone released from the stomach, is associated with cardioprotection. Read More

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http://dx.doi.org/10.1007/s00395-020-0809-zDOI Listing

Nuclear localization of a novel calpain-2 mediated junctophilin-2 C-terminal cleavage peptide promotes cardiomyocyte remodeling.

Basic Res Cardiol 2020 Jun 26;115(4):49. Epub 2020 Jun 26.

Cardiovascular Research Institute, Baylor College of Medicine, One Baylor Plaza, BCM335, Houston, TX, 77030, USA.

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. Patients with HF exhibit a loss of junctophilin-2 (JPH2), a structural protein critical in forming junctional membrane complexes in which excitation-contraction takes place. Several mechanisms have been proposed to mediate the loss of JPH2, one being cleavage by the calcium-dependent protease calpain. Read More

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http://dx.doi.org/10.1007/s00395-020-0807-1DOI Listing

Secreted frizzled-related protein 2, a novel mechanism to induce myocardial ischemic protection through angiogenesis.

Basic Res Cardiol 2020 Jun 26;115(4):48. Epub 2020 Jun 26.

Department of Cell Biology & Molecular Medicine, New Jersey Medical School, Rutgers University-New Jersey Medical School, Newark, NJ, USA.

Our hypothesis is that Secreted Frizzled-Related Protein 2 (sFPR2) is an important mechanism mediating ischemic cardioprotection, since it is the most upregulated gene in the third window of ischemic preconditioning. One week after permanent coronary artery occlusion (CAO), sFRP2 TG mice exhibited a 49% higher LV ejection fraction and a 36% reduction in infarct size, p < 0.05, and reduced fibrosis in both adjacent and remote zones, along with an increase in collagen type III and a decrease in the collagen type I/III ratio compared with WTL. Read More

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http://dx.doi.org/10.1007/s00395-020-0808-0DOI Listing

Deficiency of Nucleotide-binding oligomerization domain-containing proteins (NOD) 1 and 2 reduces atherosclerosis.

Basic Res Cardiol 2020 Jun 25;115(4):47. Epub 2020 Jun 25.

Cardiology and Angiology, Philipps-University Marburg, Hans-Meerwein-Straße 2, 35043, Marburg, Germany.

Atherosclerosis is crucially fueled by inflammatory pathways including pattern recognition receptor (PRR)-related signaling of the innate immune system. Currently, the impact of the cytoplasmic PRRs nucleotide-binding oligomerization domain-containing protein (NOD) 1 and 2 is incompletely characterized. We, therefore, generated Nod1/Nod2 double knockout mice on a low-density lipoprotein receptor (Ldlr)-deficient background (= LdlrNod1/2) which were subsequently analyzed regarding experimental atherosclerosis, lipid metabolism, insulin resistance and gut microbiota composition. Read More

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http://dx.doi.org/10.1007/s00395-020-0806-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7316681PMC

The inotropic agent digitoxin strengthens desmosomal adhesion in cardiac myocytes in an ERK1/2-dependent manner.

Basic Res Cardiol 2020 Jun 17;115(4):46. Epub 2020 Jun 17.

Faculty of Medicine, Ludwig-Maximilians-Universität (LMU) Munich, Pettenkoferstraße 11, 80336, Munich, Germany.

Desmosomal proteins are components of the intercalated disc and mediate cardiac myocyte adhesion. Enhancement of cardiac myocyte cohesion, referred to as "positive adhesiotropy", was demonstrated to be a function of sympathetic signaling and to be relevant for a sufficient inotropic response. We used the inotropic agent digitoxin to investigate the link between inotropy and adhesiotropy. Read More

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http://dx.doi.org/10.1007/s00395-020-0805-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7299919PMC

Deletion of newly described pro-survival molecule Pellino-1 increases oxidative stress, downregulates cIAP2/NF-κB cell survival pathway, reduces angiogenic response, and thereby aggravates tissue function in mouse ischemic models.

Basic Res Cardiol 2020 Jun 14;115(4):45. Epub 2020 Jun 14.

Department of Surgery, Molecular Cardiology and Angiogenesis Laboratory, University of Connecticut School of Medicine, University of Connecticut Health, Farmington, 06030, CT, USA.

Introduction: In the present study, we aimed to explore the functional role of Pellino-1 (Peli1) in inducing neovascularization after myocardial infarction (MI) and hindlimb ischemia (HLI) using Peli1 global knockout mice (Peli1). Recently we have shown that Peli1, an E3 ubiquitin ligase, induce angiogenesis and improve survivability, with decreased necrosis of ischemic skin flaps.

Methods: Peli1 and Peli1 mice were subjected to either permanent ligation of the left anterior descending coronary artery (LAD) or sham surgery (S). Read More

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http://dx.doi.org/10.1007/s00395-020-0804-4DOI Listing

Anaemia is associated with severe RBC dysfunction and a reduced circulating NO pool: vascular and cardiac eNOS are crucial for the adaptation to anaemia.

Basic Res Cardiol 2020 Jun 12;115(4):43. Epub 2020 Jun 12.

Department of Cardiology, Pulmonary Diseases, and Vascular Medicine, Medical Faculty, CARID Cardiovascular Research Institute of Duesseldorf, Heinrich Heine University of Duesseldorf, Moorenstr. 5, 40225, Düsseldorf, Germany.

Anaemia is frequently present in patients with acute myocardial infarction (AMI) and contributes to an adverse prognosis. We hypothesised that, besides reduced oxygen carrying capacity, anaemia is associated with (1) red blood cell (RBC) dysfunction and a reduced circulating nitric oxide (NO) pool, (2) compensatory enhancement of vascular and cardiac endothelial nitric oxide synthase (eNOS) activity, and (3) contribution of both, RBC dysfunction and reduced circulatory NO pool to left ventricular (LV) dysfunction and fatal outcome in AMI. In mouse models of subacute and chronic anaemia from repeated mild blood loss the circulating NO pool, RBC, cardiac and vascular function were analysed at baseline and in reperfused AMI. Read More

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http://dx.doi.org/10.1007/s00395-020-0799-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7293199PMC

Interplay of the red blood cell and vascular endothelial nitric oxide synthase system to combat cardiac complications of anemia.

Basic Res Cardiol 2020 Jun 12;115(4):44. Epub 2020 Jun 12.

Center for Cardiology, Cardiology I, University Medical Center Mainz, Geb. 605, Langenbeckstr. 1, 55131, Mainz, Germany.

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http://dx.doi.org/10.1007/s00395-020-0801-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7292806PMC

Inflammation shapes pathogenesis of murine arrhythmogenic cardiomyopathy.

Basic Res Cardiol 2020 Jun 12;115(4):42. Epub 2020 Jun 12.

Institute of Molecular and Cellular Anatomy, RWTH Aachen University, 52074, Aachen, Germany.

Arrhythmogenic cardiomyopathy (AC) is an incurable genetic disease, whose pathogenesis is poorly understood. AC is characterized by arrhythmia, fibrosis, and cardiodilation that may lead to sudden cardiac death or heart failure. To elucidate AC pathogenesis and to design possible treatment strategies of AC, multiple murine models have been established. Read More

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http://dx.doi.org/10.1007/s00395-020-0803-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289786PMC

Vascular autophagy in health and disease.

Basic Res Cardiol 2020 Jun 6;115(4):41. Epub 2020 Jun 6.

Department of Medicine, Cardiovascular Center, Medical College of Wisconsin, 8701 West Watertown Plank Road, Milwaukee, WI, 53213, USA.

Homeostasis is maintained within organisms through the physiological recycling process of autophagy, a catabolic process that is intricately involved in the mobilization of nutrients during starvation, recycling of cellular cargo, as well as initiation of cellular death pathways. Specific to the cardiovascular system, autophagy responds to both chemical (e.g. Read More

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http://dx.doi.org/10.1007/s00395-020-0802-6DOI Listing

Intravenously delivered mesenchymal stem cells prevent microvascular obstruction formation after myocardial ischemia/reperfusion injury.

Basic Res Cardiol 2020 May 25;115(4):40. Epub 2020 May 25.

Department of Cardiology, Drum Tower Hospital, State Key Laboratory of Pharmaceutical Biotechnology, Medical School of Nanjing University, No. 321 Zhongshan Road, Nanjing, 210008, China.

Microvascular obstruction (MVO) after primary percutaneous coronary intervention (pPCI) is identified as an independent risk factor for poor prognosis in patients with acute myocardial infarction (AMI). The inflammatory response induced by ischemia and reperfusion (I/R) injury is considered one of the main mechanisms of MVO. Mesenchymal stem cells (MSCs) are a unique stromal cell type that confers an immunomodulatory effect in cardiac disease. Read More

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http://dx.doi.org/10.1007/s00395-020-0800-8DOI Listing

Microvascular and lymphatic dysfunction in HFpEF and its associated comorbidities.

Basic Res Cardiol 2020 May 25;115(4):39. Epub 2020 May 25.

Institut National de la Santé et de la Recherche Médicale (Inserm) UMR1096, Faculty of Medicine and Pharmacy, Normandy University, 22 Boulevard Gambetta, 76183, Rouen, France.

Heart failure with preserved ejection fraction (HFpEF) is a complex heterogeneous disease for which our pathophysiological understanding is still limited and specific prevention and treatment strategies are lacking. HFpEF is characterised by diastolic dysfunction and cardiac remodelling (fibrosis, inflammation, and hypertrophy). Recently, microvascular dysfunction and chronic low-grade inflammation have been proposed to participate in HFpEF development. Read More

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http://dx.doi.org/10.1007/s00395-020-0798-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7248044PMC

Increased RyR2 activity is exacerbated by calcium leak-induced mitochondrial ROS.

Basic Res Cardiol 2020 May 22;115(4):38. Epub 2020 May 22.

Dorothy M. Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Columbus, OH, 43210, USA.

Cardiac disease is associated with deleterious emission of mitochondrial reactive oxygen species (mito-ROS), as well as enhanced oxidation and activity of the sarcoplasmic reticulum (SR) Ca release channel, the ryanodine receptor (RyR2). The transfer of Ca from the SR via RyR2 to mitochondria is thought to play a key role in matching increased metabolic demand during stress. In this study, we investigated whether augmented RyR2 activity results in self-imposed exacerbation of SR Ca leak, via altered SR-mitochondrial Ca transfer and elevated mito-ROS emission. Read More

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http://dx.doi.org/10.1007/s00395-020-0797-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244455PMC

Longitudinal metabolic profiling of cardiomyocytes derived from human-induced pluripotent stem cells.

Basic Res Cardiol 2020 May 18;115(4):37. Epub 2020 May 18.

Department of Internal Medicine I, Division of Cardiology, University Hospital Jena, FSU, FZL Haus F4, Am Klinikum 1, 07747, Jena, Germany.

Human-induced pluripotent stem cells (h-iPSCs) are a unique in vitro model for cardiovascular research. To realize the potential applications of h-iPSCs-derived cardiomyocytes (CMs) for drug testing or regenerative medicine and disease modeling, characterization of the metabolic features is critical. Here, we show the transcriptional profile during stages of cardiomyogenesis of h-iPSCs-derived CMs. Read More

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http://dx.doi.org/10.1007/s00395-020-0796-0DOI Listing

Allogeneic cardiosphere-derived cells (CAP-1002) in critically ill COVID-19 patients: compassionate-use case series.

Basic Res Cardiol 2020 05 12;115(4):36. Epub 2020 May 12.

Cedars-Sinai Medical Center, Smidt Heart Institute, 127 S. San Vicente Boulevard, Advanced Health Sciences Pavilion, Third Floor, Suite A3100, Los Angeles, CA, 90048, USA.

There are no definitive therapies for patients with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. Therefore, new therapeutic strategies are needed to improve clinical outcomes, particularly in patients with severe disease. This case series explores the safety and effectiveness of intravenous allogeneic cardiosphere-derived cells (CDCs), formulated as CAP-1002, in critically ill patients with confirmed coronavirus disease 2019 (COVID-19). Read More

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http://dx.doi.org/10.1007/s00395-020-0795-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214858PMC

A future for remote ischaemic conditioning in high-risk patients.

Basic Res Cardiol 2020 Apr 25;115(3):35. Epub 2020 Apr 25.

The Hatter Cardiovascular Institute, University College London, London, UK.

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http://dx.doi.org/10.1007/s00395-020-0794-2DOI Listing

The endocannabinoid anandamide has an anti-inflammatory effect on CCL2 expression in vascular smooth muscle cells.

Basic Res Cardiol 2020 Apr 22;115(3):34. Epub 2020 Apr 22.

Fachbereich Medizin, Institute for Cardiovascular Physiology, Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.

Endocannabinoids are important lipid-signaling mediators. Both protective and deleterious effects of endocannabinoids in the cardiovascular system have been reported but the mechanistic basis for these contradicting observations is unclear. We set out to identify anti-inflammatory mechanisms of endocannabinoids in the murine aorta and in human vascular smooth muscle cells (hVSMC). Read More

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http://dx.doi.org/10.1007/s00395-020-0793-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7176595PMC

Translational large animal model of hibernating myocardium: characterization by serial multimodal imaging.

Basic Res Cardiol 2020 Apr 14;115(3):33. Epub 2020 Apr 14.

Translational Laboratory for Cardiovascular Imaging and Therapy, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), C/ Melchor Fernandez Almagro 3, Madrid, 28029, Spain.

Nonrevascularizable coronary artery disease is a frequent cause of hibernating myocardium leading to heart failure (HF). Currently, there is a paucity of therapeutic options for patients with this condition. There is a lack of animal models resembling clinical features of hibernating myocardium. Read More

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http://dx.doi.org/10.1007/s00395-020-0788-0DOI Listing
April 2020
5.414 Impact Factor

Perspective: cardiovascular disease and the Covid-19 pandemic.

Basic Res Cardiol 2020 04 10;115(3):32. Epub 2020 Apr 10.

Department of Cardiology, Universitätsmedizin Mainz and DZHK Standort Rhein-Main, Langenbeckstrasse 1, 55131, Mainz, Germany.

We summarize the cardiovascular risks associated with Covid-19 pandemic, discussing the risks for both infected and non-infected patients. Read More

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http://dx.doi.org/10.1007/s00395-020-0792-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7146013PMC

COVID-19 in the heart and the lungs: could we "Notch" the inflammatory storm?

Basic Res Cardiol 2020 04 9;115(3):31. Epub 2020 Apr 9.

Maria Cecilia Hospital, GVM Care & Research, Cotignola, Italy.

From January 2020, coronavirus disease (COVID-19) originated in China has spread around the world. The disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The presence of myocarditis, cardiac arrest, and acute heart failure in COVID-19 patients suggests the existence of a relationship between SARS-CoV-2 infection and cardiac disease. Read More

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http://dx.doi.org/10.1007/s00395-020-0791-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7144545PMC

Matrix metalloproteinase-7 in platelet-activated macrophages accounts for cardiac remodeling in uremic mice.

Basic Res Cardiol 2020 Apr 9;115(3):30. Epub 2020 Apr 9.

Kidney Institution of the Chinese People's Liberation Army, Chang Zheng Hospital, the Second Military Medical University, Feng Yang Road, No. 415, Huangpu District, Shanghai, China.

Heart failure is the leading cause of mortality in patients with end-stage renal disease, and progressive cardiac remodeling is the key pathological basis of heart failure. However, the mechanism by which uremia-induced cardiac remodeling occurs is not well understood. Here, we showed that platelets were significantly activated in 5/6 nephrectomy-operated mice, and cardiac remodeling in the uremic mice was significantly improved when platelets were effectively depleted. Read More

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http://dx.doi.org/10.1007/s00395-020-0789-zDOI Listing
April 2020
5.414 Impact Factor

CARD9 promotes autophagy in cardiomyocytes in myocardial ischemia/reperfusion injury via interacting with Rubicon directly.

Basic Res Cardiol 2020 Apr 4;115(3):29. Epub 2020 Apr 4.

Department of Pathophysiology, Sepsis Translational Medicine Key Lab of Hunan Province, Xiangya School of Medicine, Central South University, Changsha, 410000, Hunan, China.

Autophagy in cardiomyocyte is involved in myocardial ischemia/reperfusion (M-I/R) injury. Caspase recruitment domain-containing protein 9 (CARD9) plays a critical role in cardiovascular diseases (CVDs) such as hypertension and cardiac fibrosis. However, its role in autophagy following M-I/R injury is yet to be fully elucidated. Read More

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http://dx.doi.org/10.1007/s00395-020-0790-6DOI Listing

Exercise improves cardiac function and glucose metabolism in mice with experimental myocardial infarction through inhibiting HDAC4 and upregulating GLUT1 expression.

Basic Res Cardiol 2020 Mar 31;115(3):28. Epub 2020 Mar 31.

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China.

This study aims to determine the effect of exercise on the cardiac function, metabolic profiles and related molecular mechanisms in mice with ischemic-induced heart failure (HF). HF was induced by myocardial infarction (MI) in C57BL6/N mice. Cardiac function and physical endurance were improved in HF mice after exercise. Read More

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http://dx.doi.org/10.1007/s00395-020-0787-1DOI Listing
March 2020
5.414 Impact Factor

Correction to: DNA‑PKcs promotes cardiac ischemia reperfusion injury through mitigating BI‑1‑governed mitochondrial homeostasis.

Basic Res Cardiol 2020 03 6;115(3):25. Epub 2020 Mar 6.

Department of Cardiology and Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.

Since the publication of the article, the authors found a small problem with Fig. 7e. Unfortunately, Fig. Read More

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http://dx.doi.org/10.1007/s00395-020-0786-2DOI Listing
March 2020
5.414 Impact Factor

Small extracellular vesicles secreted from human amniotic fluid mesenchymal stromal cells possess cardioprotective and promigratory potential.

Basic Res Cardiol 2020 03 7;115(3):26. Epub 2020 Mar 7.

The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.

Mesenchymal stromal cells (MSCs) exhibit antiapoptotic and proangiogenic functions in models of myocardial infarction which may be mediated by secreted small extracellular vesicles (sEVs). However, MSCs have frequently been harvested from aged or diseased patients, while the isolated sEVs often contain high levels of impurities. Here, we studied the cardioprotective and proangiogenic activities of size-exclusion chromatography-purified sEVs secreted from human foetal amniotic fluid stem cells (SS-hAFSCs), possessing superior functional potential to that of adult MSCs. Read More

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http://dx.doi.org/10.1007/s00395-020-0785-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060967PMC

CRISPLD1: a novel conserved target in the transition to human heart failure.

Basic Res Cardiol 2020 03 7;115(3):27. Epub 2020 Mar 7.

Laboratory of Experimental Cardiology, Clinic for Cardiology and Pneumology, Heart Research Center, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany.

Heart failure is a major health problem worldwide with a significant morbidity and mortality rate. Although studied extensively in animal models, data from patients at the compensated disease stage are lacking. We sampled myocardium biopsies from aortic stenosis patients with compensated hypertrophy and moderate heart failure and used transcriptomics to study the transition to failure. Read More

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http://dx.doi.org/10.1007/s00395-020-0784-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7060963PMC

Action of iron chelator on intramyocardial hemorrhage and cardiac remodeling following acute myocardial infarction.

Basic Res Cardiol 2020 03 5;115(3):24. Epub 2020 Mar 5.

Physical Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada.

Intramyocardial hemorrhage is an independent predictor of adverse outcomes in ST-segment elevation myocardial infarction (STEMI). Iron deposition resulting from ischemia-reperfusion injury (I/R) is pro-inflammatory and has been associated with adverse remodeling. The role of iron chelation in hemorrhagic acute myocardial infarction (AMI) has never been explored. Read More

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http://dx.doi.org/10.1007/s00395-020-0782-6DOI Listing
March 2020
5.414 Impact Factor

Mitochondrial noncoding RNA-regulatory network in cardiovascular disease.

Basic Res Cardiol 2020 03 5;115(3):23. Epub 2020 Mar 5.

Cardiovascular Research Unit, Luxembourg Institute of Health, 1A-B rue Edison, 1445, Strassen, Luxembourg.

Mitochondrial function and integrity are vital for the maintenance of cellular homeostasis, particularly in high-energy demanding cells. Cardiomyocytes have a large number of mitochondria, which provide a continuous and bulk supply of the ATP necessary for cardiac mechanical function. More than 90% of the ATP consumed by the heart is derived from the mitochondrial oxidative metabolism. Read More

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http://dx.doi.org/10.1007/s00395-020-0783-5DOI Listing

M1-like macrophage-derived exosomes suppress angiogenesis and exacerbate cardiac dysfunction in a myocardial infarction microenvironment.

Basic Res Cardiol 2020 02 28;115(2):22. Epub 2020 Feb 28.

Guangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, Guangdong, People's Republic of China.

The roles and the underlying mechanisms of M1-type macrophages in angiogenesis and postmyocardial infarction (MI) cardiac repair have remained unclear. In this study, we investigated the role of M1-like macrophage-derived exosomes in a MI microenvironment. We found that the proinflammatory M1-like-type macrophages released an extensive array of proinflammatory exosomes (M1-Exos) after MI. Read More

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http://dx.doi.org/10.1007/s00395-020-0781-7DOI Listing
February 2020
5.414 Impact Factor

Perturbations in myocardial perfusion and oxygen balance in swine with multiple risk factors: a novel model of ischemia and no obstructive coronary artery disease.

Basic Res Cardiol 2020 02 25;115(2):21. Epub 2020 Feb 25.

Division of Experimental Cardiology, Department of Cardiology, Thoraxcenter, Erasmus MC, University Medical Center Rotterdam, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.

Comorbidities of ischemic heart disease, including diabetes mellitus (DM), hypercholesterolemia (HC) and chronic kidney disease (CKD), are associated with coronary microvascular dysfunction (CMD). Increasing evidence suggests that CMD may contribute to myocardial 'Ischemia and No Obstructive Coronary Artery disease' (INOCA). In the present study, we tested the hypothesis that CMD results in perturbations in myocardial perfusion and oxygen delivery using a novel swine model with multiple comorbidities. Read More

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http://dx.doi.org/10.1007/s00395-020-0778-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7042191PMC
February 2020

Inhibition of Na1.8 prevents atrial arrhythmogenesis in human and mice.

Basic Res Cardiol 2020 02 20;115(2):20. Epub 2020 Feb 20.

Department of Internal Medicine II, University Medical Center Regensburg, Franz-Josef-Strauß-Allee 11, 93053, Regensburg, Germany.

Pharmacologic approaches for the treatment of atrial arrhythmias are limited due to side effects and low efficacy. Thus, the identification of new antiarrhythmic targets is of clinical interest. Recent genome studies suggested an involvement of SCN10A sodium channels (Na1. Read More

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http://dx.doi.org/10.1007/s00395-020-0780-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7033079PMC
February 2020

Triad3A attenuates pathological cardiac hypertrophy involving the augmentation of ubiquitination-mediated degradation of TLR4 and TLR9.

Basic Res Cardiol 2020 02 1;115(2):19. Epub 2020 Feb 1.

Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center For Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, 211166, China.

Activation of TLRs mediated the NF-κB signaling pathway plays an important pathophysiological role in cardiac hypertrophy. Triad3A, a ubiquitin E3 ligase, has been reported to negatively regulate NF-κB activation pathway via promoting ubiquitination and degradation of TLR4 and TLR9 in innate immune cells. The role of Triad3A in cardiac hypertrophic development remains unknown. Read More

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http://dx.doi.org/10.1007/s00395-020-0779-1DOI Listing
February 2020
5.414 Impact Factor

Murine sca1/flk1-positive cells are not endothelial progenitor cells, but B2 lymphocytes.

Basic Res Cardiol 2020 01 24;115(2):18. Epub 2020 Jan 24.

Westdeutsches Herz- und Gefäßzentrum, Klinik für Kardiologie und Angiologie, Universitätsklinikum Essen, Essen, Germany.

Circulating sca1/flk1 cells are hypothesized to be endothelial progenitor cells (EPCs) in mice that contribute to atheroprotection by replacing dysfunctional endothelial cells. Decreased numbers of circulating sca1/flk1 cells correlate with increased atherosclerotic lesions and impaired reendothelialization upon electric injury of the common carotid artery. However, legitimate doubts remain about the identity of the putative EPCs and their contribution to endothelial restoration. Read More

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http://dx.doi.org/10.1007/s00395-020-0774-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6981106PMC
January 2020

FHL-1 is not involved in pressure overload-induced maladaptive right ventricular remodeling and dysfunction.

Basic Res Cardiol 2020 01 24;115(2):17. Epub 2020 Jan 24.

Member of the German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, Aulweg 130, 35392, Giessen, Germany.

Aims: The cytoskeletal signaling protein four and-a-half LIM domains 1 (FHL-1) has recently been identified as a novel key player in pulmonary hypertension as well as in left heart diseases. In this regard, FHL-1 has been implicated in dysregulated hypertrophic signaling in pulmonary arterial smooth muscle cells leading to pulmonary hypertension. In mice, FHL-1-deficiency (FHL-1) led to an attenuated hypertrophic signaling associated with a blunted hypertrophic response of the pressure-overloaded left ventricle (LV). Read More

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http://dx.doi.org/10.1007/s00395-019-0767-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6981327PMC
January 2020

Selective intrarenal delivery of mesenchymal stem cell-derived extracellular vesicles attenuates myocardial injury in experimental metabolic renovascular disease.

Basic Res Cardiol 2020 01 14;115(2):16. Epub 2020 Jan 14.

Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, 55905, USA.

Extracellular vesicles (EVs) deliver genes and proteins to recipient cells, and mediate paracrine actions of their parent cells. Intrarenal delivery of mesenchymal stem cell (MSC)-derived EVs preserves stenotic-kidney function and reduces release of pro-inflammatory cytokines in a swine model of coexisting metabolic syndrome (MetS) and renal artery stenosis (RAS). We hypothesized that this approach is also capable of blunting cardiac injury and dysfunction. Read More

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http://dx.doi.org/10.1007/s00395-019-0772-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7333936PMC
January 2020
5.414 Impact Factor

Renal denervation restrains the inflammatory response in myocardial ischemia-reperfusion injury.

Basic Res Cardiol 2020 01 13;115(2):15. Epub 2020 Jan 13.

Department of Cardiology, Nanjing Drum Tower Hospital, State Key Laboratory of Pharmaceutical Biotechnology, The Affiliated Hospital of Nanjing University Medical School, No. 321 Zhongshan Road, Nanjing, 210008, China.

Myocardial ischemia-reperfusion (I/R) injury leads to intensive sympathetic nervous system (SNS) activation and inflammatory reactions. Whether renal sympathetic denervation (RDN) could be a new therapeutic strategy to modulate I/R inflammation and reduce infarct size after myocardial I/R injury needs to be explored. First, we investigated the correlation between plasma norepinephrine concentrations and circulating myeloid cell numbers in patients with acute myocardial infarction. Read More

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http://dx.doi.org/10.1007/s00395-020-0776-4DOI Listing
January 2020

TRPV4 deletion protects heart from myocardial infarction-induced adverse remodeling via modulation of cardiac fibroblast differentiation.

Basic Res Cardiol 2020 01 10;115(2):14. Epub 2020 Jan 10.

Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH, 44272, USA.

Cardiac fibrosis caused by adverse cardiac remodeling following myocardial infarction can eventually lead to heart failure. Although the role of soluble factors such as TGF-β is well studied in cardiac fibrosis following myocardial injury, the physiological role of mechanotransduction is not fully understood. Here, we investigated the molecular mechanism and functional role of TRPV4 mechanotransduction in cardiac fibrosis. Read More

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http://dx.doi.org/10.1007/s00395-020-0775-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7322630PMC
January 2020

Overexpression of mitochondrial creatine kinase preserves cardiac energetics without ameliorating murine chronic heart failure.

Basic Res Cardiol 2020 01 10;115(2):12. Epub 2020 Jan 10.

Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.

Mitochondrial creatine kinase (Mt-CK) is a major determinant of cardiac energetic status and is down-regulated in chronic heart failure, which may contribute to disease progression. We hypothesised that cardiomyocyte-specific overexpression of Mt-CK would mitigate against these changes and thereby preserve cardiac function. Male Mt-CK overexpressing mice (OE) and WT littermates were subjected to transverse aortic constriction (TAC) or sham surgery and assessed by echocardiography at 0, 3 and 6 weeks alongside a final LV haemodynamic assessment. Read More

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http://dx.doi.org/10.1007/s00395-020-0777-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6954138PMC
January 2020

Tryptophane-kynurenine pathway in the remote ischemic conditioning mechanism.

Basic Res Cardiol 2020 01 10;115(2):13. Epub 2020 Jan 10.

Institut Mitovasc, UMR CNRS 6015, INSERM U1083, CHU d'Angers, Université d'Angers, Angers, France.

The actual protective mechanisms underlying cardioprotection with remote ischemic conditioning (RIC) remain unclear. Recent data suggest that RIC induces kynurenine (KYN) and kynurenic acid synthesis, two metabolites derived from tryptophan (TRP), yet a causal relation between TRP pathway and RIC remains to be established. We sought to study the impact of RIC on the levels of TRP and its main metabolites within tissues, and to assess whether blocking kynurenine (KYN) synthesis from TRP would inhibit RIC-induced cardioprotection. Read More

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http://dx.doi.org/10.1007/s00395-019-0770-xDOI Listing
January 2020

DNA-PKcs promotes cardiac ischemia reperfusion injury through mitigating BI-1-governed mitochondrial homeostasis.

Basic Res Cardiol 2020 01 9;115(2):11. Epub 2020 Jan 9.

Department of Cardiology and Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.

DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is a novel inducer to promote mitochondrial apoptosis and suppress tumor growth in a variety of cells although its role in cardiovascular diseases remains obscure. This study was designed to examine the role of DNA-PKcs in cardiac ischemia reperfusion (IR) injury and mitochondrial damage. Cardiomyocyte-specific DNA-PKcs knockout (DNA-PKcs) mice were subjected to IR prior to assessment of myocardial function and mitochondrial apoptosis. Read More

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http://dx.doi.org/10.1007/s00395-019-0773-7DOI Listing
January 2020
5.414 Impact Factor

Thrombin receptor PAR4 drives canonical NLRP3 inflammasome signaling in the heart.

Basic Res Cardiol 2020 01 7;115(2):10. Epub 2020 Jan 7.

Institute of Pharmacology, West German Heart and Vascular Center, Medical Faculty, University Duisburg-Essen, Hufelandstr. 55, 45122, Essen, Germany.

The deleterious effects of diabetes in the heart are increasingly attributed to inflammatory signaling through the NLRP3 (NOD, LRR and PYD domains-containing protein 3) inflammasome. Thrombin antagonists reduce cardiac remodeling and dysfunction in diabetic mice, in part by suppressing fibrin-driven inflammation. The role of cellular thrombin receptor subtypes in this context is not known. Read More

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http://dx.doi.org/10.1007/s00395-019-0771-9DOI Listing
January 2020

Fibroblast growth factor 21 inhibited ischemic arrhythmias via targeting miR-143/EGR1 axis.

Basic Res Cardiol 2020 01 4;115(2). Epub 2020 Jan 4.

Department of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Medicine Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, 150081, China.

Ventricular arrhythmia is the most common cause of sudden cardiac death in patients with myocardial infarction (MI). Fibroblast growth factor 21 (FGF21) has been shown to play an important role in cardiovascular and metabolic diseases. However, the effects of FGF21 on ventricular arrhythmias following MI have not been addressed yet. Read More

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http://dx.doi.org/10.1007/s00395-019-0768-4DOI Listing
January 2020

Distinct origins and functions of cardiac orthotopic macrophages.

Basic Res Cardiol 2020 01 2;115(2). Epub 2020 Jan 2.

Department of Cardiology, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, Zhejiang, P.R. China.

Macrophages are one cell type in the innate immune system. Recent studies involving macrophages have overturned the conventional concept that circulating bone marrow-derived blood mononuclear cells in the adult body continuously replace macrophages residing in the tissues. Investigations using refined technologies have suggested that embryonic hematopoiesis can result in the differentiation into macrophage subgroups in some tissues. Read More

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http://dx.doi.org/10.1007/s00395-019-0769-3DOI Listing
January 2020
5.414 Impact Factor

Cell shape determines gene expression: cardiomyocyte morphotypic transcriptomes.

Basic Res Cardiol 2019 12 23;115(1). Epub 2019 Dec 23.

Department of Medicine, Integrated Cardio Metabolic Centre (ICMC), Heart and Vascular Theme, Karolinska Institutet, 141 57, Huddinge, Sweden.

Cardiomyocytes undergo considerable changes in cell shape. These can be due to hemodynamic constraints, including changes in preload and afterload conditions, or to mutations in genes important for cardiac function. These changes instigate significant changes in cellular architecture and lead to the addition of sarcomeres, at the same time or at a later stage. Read More

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http://dx.doi.org/10.1007/s00395-019-0765-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928094PMC
December 2019

Heart non-specific effector CD4 T cells protect from postinflammatory fibrosis and cardiac dysfunction in experimental autoimmune myocarditis.

Basic Res Cardiol 2019 12 20;115(1). Epub 2019 Dec 20.

Department of Rheumatology, Center of Experimental Rheumatology, University Hospital Zurich, Zurich, Switzerland.

Heart-specific CD4 T cells have been implicated in development and progression of myocarditis in mice and in humans. Here, using mouse models of experimental autoimmune myocarditis (EAM) we investigated the role of heart non-specific CD4 T cells in the progression of the disease. Heart non-specific CD4 T cells were obtained from DO11. Read More

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http://dx.doi.org/10.1007/s00395-019-0766-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6925074PMC
December 2019
5.414 Impact Factor

Importance of infarct size versus other variables for clinical outcomes after PPCI in STEMI patients.

Basic Res Cardiol 2019 12 12;115(1). Epub 2019 Dec 12.

INSERM UMR 1060, CarMeN Laboratory, University Claude Bernard Lyon1, IHU OPeRa, Hôpital Louis Pradel, Hospices Civils de Lyon, 69677, Lyon, France.

Despite promising experimental studies and encouraging proof-of-concept clinical trials, interventions aimed at limiting infarct size have failed to improve clinical outcomes in patients with ST-elevation myocardial infarction (STEMI). Our objective was to examine whether variables (cardiovascular risk factors, comorbidities, post-procedural variables, cotreatments) might be associated with clinical outcomes in STEMI patients independently from infarct size reduction. The present study was based on a post hoc analysis of the CIRCUS trial database (Clinicaltrials. Read More

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http://dx.doi.org/10.1007/s00395-019-0764-8DOI Listing
December 2019

The changing face after acute myocardial infarction.

Basic Res Cardiol 2019 12 12;115(1). Epub 2019 Dec 12.

Department of Cardiology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.

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http://dx.doi.org/10.1007/s00395-019-0762-xDOI Listing
December 2019

Egr-1 functions as a master switch regulator of remote ischemic preconditioning-induced cardioprotection.

Basic Res Cardiol 2019 12 10;115(1). Epub 2019 Dec 10.

Department of Cardiology, Kolling Institute, Northern Sydney Local Health District, Level 12, Royal North Shore Hospital, Cnr Reserve Rd and Westbourne, St Leonards, NSW, 2065, Australia.

Despite improved treatment options myocardial infarction (MI) is still a leading cause of mortality and morbidity worldwide. Remote ischemic preconditioning (RIPC) is a mechanistic process that reduces myocardial infarction size and protects against ischemia reperfusion (I/R) injury. The zinc finger transcription factor early growth response-1 (Egr-1) is integral to the biological response to I/R, as its upregulation mediates the increased expression of inflammatory and prothrombotic processes. Read More

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http://dx.doi.org/10.1007/s00395-019-0763-9DOI Listing
December 2019

Molecular pathways involved in the cardioprotective effects of intravenous statin administration during ischemia.

Basic Res Cardiol 2019 11 28;115(1). Epub 2019 Nov 28.

Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB-Sant Pau, Avda. S. Antoni María Claret 167, 08025, Barcelona, Spain.

The success of therapies targeting myocardial reperfusion injury is limited, while the cardioprotective impact of mitigating ischemia-related damage remains less explored. We have recently shown in a pig model that the intravenous administration of a modified atorvastatin preparation during ischemia attenuates the rise of cardiac ischemia injury biomarkers. In the following study, we sought to investigate the mechanisms behind these ischemia-related cardioprotective effects. Read More

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http://dx.doi.org/10.1007/s00395-019-0760-zDOI Listing
November 2019

Mitochondrial connexin 43 in sex-dependent myocardial responses and estrogen-mediated cardiac protection following acute ischemia/reperfusion injury.

Basic Res Cardiol 2019 11 18;115(1). Epub 2019 Nov 18.

Department of Surgery, Indiana University School of Medicine, 950 W. Walnut Street, R2 E319, Indianapolis, IN, 46202, USA.

Preserving mitochondrial activity is crucial in rescuing cardiac function following acute myocardial ischemia/reperfusion (I/R). The sex difference in myocardial functional recovery has been observed after I/R. Given the key role of mitochondrial connexin43 (Cx43) in cardiac protection initiated by ischemic preconditioning, we aimed to determine the implication of mitochondrial Cx43 in sex-related myocardial responses and to examine the effect of estrogen (17β-estradiol, E2) on Cx43, particularly mitochondrial Cx43-involved cardiac protection following I/R. Read More

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http://dx.doi.org/10.1007/s00395-019-0759-5DOI Listing
November 2019
5.414 Impact Factor