9,940 results match your criteria Arteriosclerosis Thrombosis And Vascular Biology[Journal]


Vascular Aging and Vascular Disease Have Much in Common!

Arterioscler Thromb Vasc Biol 2022 Jun 23:101161ATVBAHA122317892. Epub 2022 Jun 23.

Atherothrombosis and Vascular Biology Program, Baker Heart and Diabetes Institute, Central Clinical School, Monash University, Melbourne, VIC, Australia. Department of Cardiometabolic Health, University of Melbourne, VIC, Australia.

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Dichotomous Roles of Smooth Muscle Cell-Derived MCP1 (Monocyte Chemoattractant Protein 1) in Development of Atherosclerosis.

Arterioscler Thromb Vasc Biol 2022 Jun 23:101161ATVBAHA122317882. Epub 2022 Jun 23.

Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville (K.M.O., R.A.D., G.K.O.).

Background: Smooth muscle cells (SMCs) in atherosclerotic plaque take on multiple nonclassical phenotypes that may affect plaque stability and, therefore, the likelihood of myocardial infarction or stroke. However, the mechanisms by which these cells affect stability are only beginning to be explored.

Methods: In this study, we investigated the contribution of inflammatory MCP1 (monocyte chemoattractant protein 1) produced by both classical Myh11 (myosin heavy chain 11) SMCs and SMCs that have transitioned through an Lgals3 (galectin 3) state in atherosclerosis using smooth muscle lineage tracing mice that label all Myh11 cells and a dual lineage tracing system that targets Lgals3-transitioned SMC only. Read More

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: Entering the Next Era.

Arterioscler Thromb Vasc Biol 2022 Jul 22;42(7):809-810. Epub 2022 Jun 22.

Diabetes Research Program, Department of Medicine, New York University Grossman, School of Medicine, NY.

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PIKfyve-Dependent Phosphoinositide Dynamics in Megakaryocyte/Platelet Granule Integrity and Platelet Functions.

Arterioscler Thromb Vasc Biol 2022 Jun 16:101161ATVBAHA122317559. Epub 2022 Jun 16.

INSERM U1297, I2MC and Université Paul Sabatier, Toulouse, France (M.C., R.M., J.-M.X., G.C., J.V., A.V., F.B., B.P., H.T., S.S.).

Background: Secretory granules are key elements for platelet functions. Their biogenesis and integrity are regulated by fine-tuned mechanisms that need to be fully characterized. Here, we investigated the role of the phosphoinositide 5-kinase PIKfyve and its lipid products, PtdIns5P (phosphatidylinositol 5 monophosphate) and PtdIns(3,5)P (phosphatidylinositol (3,5) bisphosphate) in granule homeostasis in megakaryocytes and platelets. Read More

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Epicardial Adipose Tissue Ceramides Are Related to Lipoprotein Lipase Activity in Coronary Artery Disease: Unfolding a Missing Link.

Arterioscler Thromb Vasc Biol 2022 Jun 16:101161ATVBAHA122317840. Epub 2022 Jun 16.

Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC), Departamento de Bioquímica Clínica, Laboratorio de Lípidos y Aterosclerosis, Buenos Aires, Argentina (M.B., L.S., G.B.).

Background: Epicardial adipose tissue (EAT) contributes to coronary artery disease (CAD). EAT presents a specific lipidomic signature, showing increased ceramides and other proinflammatory lipids content. Besides, LPL (lipoprotein lipase) activity in EAT would contribute to its expansion, supplying fatty acids to the tissue. Read More

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Identification of a Distinct Platelet Phenotype in the Elderly: ADP Hypersensitivity Coexists With Platelet PAR (Protease-Activated Receptor)-1 and PAR-4-Mediated Thrombin Resistance.

Arterioscler Thromb Vasc Biol 2022 Jun 16:101161ATVBAHA120316772. Epub 2022 Jun 16.

Cardiology Department, Concord Repatriation General Hospital, NSW, Australia (S.R.G., M.K., L.K.).

Background: Thrombin (via PAR [protease-activated receptor]-1 and PAR-4) and ADP (via P2Y receptors) are potent endogenous platelet activators implicated in the development of cardiovascular disease. We aimed to assess whether platelet pathways alter with aging.

Methods: We characterized platelet activity in community-dwelling volunteers (n=174) in the following age groups: (1) 20 to 30 (young); (2) 40 to 55 (middle-aged); (3) ≥70 years (elderly). Read More

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Dissecting the Heterogeneity of Human Thoracic Aortic Aneurysms Using Single-Cell Transcriptomics.

Arterioscler Thromb Vasc Biol 2022 Jun 16:101161ATVBAHA122317484. Epub 2022 Jun 16.

Department of Cardiac Surgery, University of Michigan, Ann Arbor (D.M., H.F., B.Y.).

Thoracic aortic aneurysm is a life-threatening condition caused by weakening of the thoracic aorta wall, often developing silently until dissection or rupture occurs. Despite substantial efforts in the past decade, there have been no significant therapeutic advances to prevent or clinically manage diverse forms of thoracic aortic aneurysm and dissection with the only effective treatment being surgical repair. There is an urgent need to understand intra- and inter-aneurysmal heterogeneity underlying thoracic aortic aneurysm and dissection pathogenesis. Read More

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ENPP2 (Endothelial Ectonucleotide Pyrophosphatase/Phosphodiesterase 2) Increases Atherosclerosis in Female and Male Mice.

Arterioscler Thromb Vasc Biol 2022 Jun 16:101161ATVBAHA122317682. Epub 2022 Jun 16.

Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany (E.K., R.M., M.Z., F.Z., C.G., R.T.A.M., M.B., M.N.-J., A.S.).

Background: Maladapted endothelial cells (ECs) secrete ENPP2 (ectonucleotide pyrophosphatase/phosphodiesterase 2; autotaxin)-a lysophospholipase D that generates lysophosphatidic acids (LPAs). ENPP2 derived from the arterial wall promotes atherogenic monocyte adhesion induced by generating LPAs, such as arachidonoyl-LPA (LPA20:4), from oxidized lipoproteins. Here, we aimed to determine the role of endothelial ENPP2 in the production of LPAs and atherosclerosis. Read More

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Preventing Cholesterol-Induced Perk (Protein Kinase RNA-Like Endoplasmic Reticulum Kinase) Signaling in Smooth Muscle Cells Blocks Atherosclerotic Plaque Formation.

Arterioscler Thromb Vasc Biol 2022 Jun 16:101161ATVBAHA121317451. Epub 2022 Jun 16.

Division of Medical Genetics, Department of Internal Medicine, McGovern Medical School The University of Texas Health Science Center at Houston (A.C., P.G., S.M., K.K., Z.Z., A.K., C.S.K., D.M.M.).

Background: Vascular smooth muscle cells (SMCs) undergo complex phenotypic modulation with atherosclerotic plaque formation in hyperlipidemic mice, which is characterized by de-differentiation and heterogeneous increases in the expression of macrophage, fibroblast, osteogenic, and stem cell markers. An increase of cellular cholesterol in SMCs triggers similar phenotypic changes in vitro with exposure to free cholesterol due to cholesterol entering the endoplasmic reticulum, triggering endoplasmic reticulum stress and activating Perk (protein kinase RNA-like endoplasmic reticulum kinase) signaling.

Methods: We generated an SMC-specific knockout mouse model, induced hyperlipidemia in the mice by AAV- injection, and subjected them to a high-fat diet. Read More

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Microarchitectural Changes of Cardiovascular Calcification in Response to In Vivo Interventions Using Deep-Learning Segmentation and Computed Tomography Radiomics.

Arterioscler Thromb Vasc Biol 2022 Jun 16:101161ATVBAHA122317761. Epub 2022 Jun 16.

Department of Medicine, University of California, Los Angeles. (N.R.P., K.S., S.P., M.L., L.L.D., Y.T.).

Background: Coronary calcification associates closely with cardiovascular risk, but its progress is accelerated in response to some interventions widely used to reduce risk. This paradox suggests that qualitative, not just quantitative, changes in calcification may affect plaque stability. To determine if the microarchitecture of calcification varies with aging, Western diet, statin therapy, and high intensity, progressive exercise, we assessed changes in a priori selected computed tomography radiomic features (intensity, size, shape, and texture). Read More

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Gut Microbiota, Plasma Metabolomic Profiles, and Carotid Artery Atherosclerosis in HIV Infection.

Arterioscler Thromb Vasc Biol 2022 Jun 9:101161ATVBAHA121317276. Epub 2022 Jun 9.

Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York. (Z.W., B.A.P., J.X., D.B.H., T.W., K.A., R.C.K., R.D.B., Q.Q.).

Background: Alterations in gut microbiota and blood metabolomic profiles have been implicated in HIV infection and cardiovascular disease. However, it remains unclear whether alterations in gut microbiota may contribute to disrupted host blood metabolomic profiles in relation to atherosclerosis, especially in the context of HIV infection.

Methods: We analyzed cross-sectional associations between gut microbiota features and carotid artery plaque in 361 women with or at high risk of HIV (67% HIV+), and further integrated plaque-associated microbial features with plasma lipidomic/metabolomic profiles. Read More

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Endothelial Cell Insulin Signaling Regulates CXCR4 (C-X-C Motif Chemokine Receptor 4) and Limits Leukocyte Adhesion to Endothelium.

Arterioscler Thromb Vasc Biol 2022 Jul 2;42(7):e217-e227. Epub 2022 Jun 2.

Joslin Diabetes Center and Harvard Medical School, Boston, MA (T.R., B.K., C.T.C., X.W., S.M.L., J.C.P., Q.L., K.P., G.L.K., C.R.-M.).

Background: An activated, proinflammatory endothelium is a key feature in the development of complications of obesity and type 2 diabetes and can be caused by insulin resistance in endothelial cells.

Methods: We analyzed primary human endothelial cells by RNA sequencing to discover novel insulin-regulated genes and used endothelial cell culture and animal models to characterize signaling through CXCR4 (C-X-C motif chemokine receptor 4) in endothelial cells.

Results: CXCR4 was one of the genes most potently regulated by insulin, and this was mediated by PI3K (phosphatidylinositol 3-kinase), likely through FoxO1, which bound to the CXCR4 promoter. Read More

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pH-Dependent Protonation of Histidine Residues Is Critical for Electrostatic LDL (Low-Density Lipoprotein) Binding to Human Coronary Arteries.

Arterioscler Thromb Vasc Biol 2022 Jun 2:101161ATVBAHA122317868. Epub 2022 Jun 2.

Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Sweden (L.G., M.R., L.H., M.C.L., M.L., A.J., J.B., P.F.).

Background: The initiating step in atherogenesis is the electrostatic binding of LDL (low-density lipoprotein) to proteoglycan glycosaminoglycans in the arterial intima. However, although proteoglycans are widespread throughout the intima of most coronary artery segments, LDL is not evenly distributed, indicating that LDL retention is not merely dependent on the presence of proteoglycans. We aim to identify factors that promote the interaction between LDL and the vessel wall of human coronary arteries. Read More

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Ambient Air Pollution and Atherosclerosis: A Potential Mediating Role of Sphingolipids.

Arterioscler Thromb Vasc Biol 2022 Jul 2;42(7):906-918. Epub 2022 Jun 2.

BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health (Y.X., Y.H., Y.W., J.G., H.L., T.W., X.C., W.C., Y.F., X.Q., J.W., T.Z.), Peking University, Beijing, China.

Background: The pathophysiological mechanisms of air pollution-induced atherosclerosis are incompletely understood. Sphingolipids serve as biological intermediates during atherosclerosis development by facilitating production of proatherogenic apoB (apolipoprotein B)-containing lipoproteins. We explored whether sphingolipids mediate the proatherogenic effects of air pollution. Read More

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Fibrinogen and Factor XIII in Venous Thrombosis and Thrombus Stability.

Arterioscler Thromb Vasc Biol 2022 Jun 2:101161ATVBAHA122317164. Epub 2022 Jun 2.

Department of Pathology and UNC Blood Research Center, University of North Carolina, Chapel Hill.

As the third most common vascular disease, venous thromboembolism is associated with significant mortality and morbidity. Pathogenesis underlying venous thrombosis is still not fully understood. Accumulating data suggest fibrin network structure and factor XIII-mediated crosslinking are major determinants of venous thrombus mass, composition, and stability. Read More

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Carotid Siphon Calcification Predicts the Symptomatic Progression in Branch Artery Disease With Intracranial Artery Stenosis.

Arterioscler Thromb Vasc Biol 2022 Jun 2:101161ATVBAHA122317670. Epub 2022 Jun 2.

Department of Neurology, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China. (D.H., X.Y., Y.W., S.H., D.W.).

Background: Arterial calcification in the aortic arch, carotid bifurcation, or siphon on computed tomography was associated with cardiovascular disease. The association between arterial calcification prevalence and progression of branch atheromatous disease (BAD) in intracranial artery atherosclerosis was little investigated.

Methods: This study included 310 patients with ischemic stroke from one stroke center. Read More

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Promise of a Novel Bedside-to-Bench Paradigm: Can Percutaneous Coronary Intervention Proteomics Balloon Into Clinical Practice?

Arterioscler Thromb Vasc Biol 2022 Jul 26;42(7):865-867. Epub 2022 May 26.

From the Center for Interdisciplinary Cardiovascular Sciences (J.L.D., M.A., S.A.S.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.

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Distinct GEFs Couple S1PR1 to Rac for Endothelial Barrier Enhancement and Lymphocyte Trafficking.

Arterioscler Thromb Vasc Biol 2022 Jul 26;42(7):903-905. Epub 2022 May 26.

From the Université Paris Cité, Inserm, PARCC, F-75015 Paris, France.

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Function of TGFβ (Transforming Growth Factor-β) Receptor in the Vein Is Not in Vain.

Arterioscler Thromb Vasc Biol 2022 Jul 26;42(7):884-885. Epub 2022 May 26.

Department of Physiology, Cardiovascular Research Center, University of Alberta, Edmonton, Canada.

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The Remnant Lipoprotein Hypothesis of Diabetes-Associated Cardiovascular Disease.

Arterioscler Thromb Vasc Biol 2022 Jul 26;42(7):819-830. Epub 2022 May 26.

Department of Medicine, Division of Metabolism, Endocrinology and Nutrition and Department of Laboratory Medicine and Pathology, University of Washington Medicine Diabetes Institute, Seattle.

Both type 1 and type 2 diabetes are associated with an increased risk of atherosclerotic cardiovascular disease (CVD). Research based on human-first or bedside-to-bench approaches has provided new insights into likely mechanisms behind this increased risk. Although both forms of diabetes are associated with hyperglycemia, it is becoming increasingly clear that altered lipoprotein metabolism also plays a critical role in predicting CVD risk in people with diabetes. Read More

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Large Vessel Cell Heterogeneity and Plasticity: Focus in Aortic Aneurysms.

Arterioscler Thromb Vasc Biol 2022 Jul 19;42(7):811-818. Epub 2022 May 19.

A.I. Virtanen Institute for Molecular Sciences (S.J., M.K., J.P.L.), University of Eastern Finland, Kuopio.

Smooth muscle cells and endothelial cells have a remarkable level of plasticity in vascular pathologies. In thoracic and abdominal aortic aneurysms, smooth muscle cells have been suggested to undergo phenotypic switching and to contribute to degradation of the aortic wall structure in response to, for example, inflammatory mediators, dysregulation of growth factor signaling or oxidative stress. Recently, endothelial-to-mesenchymal transition, and a clonal expansion of degradative smooth muscle cells and immune cells, as well as mesenchymal stem-like cells have been suggested to contribute to the progression of aortic aneurysms. Read More

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Lack of ApoA-I in ApoEKO Mice Causes Skin Xanthomas, Worsening of Inflammation, and Increased Coronary Atherosclerosis in the Absence of Hyperlipidemia.

Arterioscler Thromb Vasc Biol 2022 Jul 19;42(7):839-856. Epub 2022 May 19.

Department of Pharmacological and Biomolecular Sciences (M.B., S.M., A.C., E.F., F.B., R.O., A.L., G.D.N., G.C.), Università degli Studi di Milano, Italy.

Background: HDL (high-density lipoprotein) and its major protein component, apoA-I (apolipoprotein A-I), play a unique role in cholesterol homeostasis and immunity. ApoA-I deficiency in hyperlipidemic, atheroprone mice was shown to drive cholesterol accumulation and inflammatory cell activation/proliferation. The present study was aimed at investigating the impact of apoA-I deficiency on lipid deposition and local/systemic inflammation in normolipidemic conditions. Read More

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Role of Sclerostin in Cardiovascular Disease.

Arterioscler Thromb Vasc Biol 2022 Jul 12;42(7):e187-e202. Epub 2022 May 12.

Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry (J.G., S.T.), James Cook University, Townsville, Queensland, Australia.

Sclerostin is most recognized for its role in controlling bone formation but is also expressed in the heart, aorta, coronary, and peripheral arteries. This review summarizes research on sclerostin's role in cardiovascular disease. Rodent studies have found sclerostin to be expressed at sites of arterial calcification. Read More

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Single-Cell Behavior in Closure of the Arterial Duct.

Arterioscler Thromb Vasc Biol 2022 Jun 5;42(6):743-744. Epub 2022 May 5.

Department of Clinical Medicine, Aarhus University, Denmark (J.A.-J., J.F.B.).

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Aging Alters the Aortic Proteome in Health and Thoracic Aortic Aneurysm.

Arterioscler Thromb Vasc Biol 2022 May 5:101161ATVBAHA122317643. Epub 2022 May 5.

Department of Internal Medicine, University of Michigan, Ann Arbor. (D.J.T., J.C., B.Y.L., S.C.W., D.R.G.).

Background: Aging enhances most chronic diseases but its impact on human aortic tissue in health and in thoracic aortic aneurysms (TAA) remains unclear.

Methods: We employed a human aortic biorepository of healthy specimens (n=17) and those that underwent surgical repair for TAA (n=20). First, we performed proteomics comparing aortas of healthy donors to aneurysmal specimens, in young (ie, <60 years of age) and old (ie, ≥60 years of age) subjects. Read More

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Endothelial Cell TGF-β (Transforming Growth Factor-Beta) Signaling Regulates Venous Adaptive Remodeling to Improve Arteriovenous Fistula Patency.

Arterioscler Thromb Vasc Biol 2022 Jul 5;42(7):868-883. Epub 2022 May 5.

Vascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.

Background: Arteriovenous fistulae (AVF) are the gold standard for vascular access for hemodialysis. Although the vein must thicken and dilate for successful hemodialysis, excessive wall thickness leads to stenosis causing AVF failure. Since TGF-β (transforming growth factor-beta) regulates ECM (extracellular matrix) deposition and smooth muscle cell (SMC) proliferation-critical components of wall thickness-we hypothesized that disruption of TGF-β signaling prevents excessive wall thickening during venous remodeling. Read More

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Leu22_Leu23 Duplication at the Signal Peptide of PCSK9 Promotes Intracellular Degradation of LDLr and Autosomal Dominant Hypercholesterolemia.

Arterioscler Thromb Vasc Biol 2022 Jul 5;42(7):e203-e216. Epub 2022 May 5.

Biofisika Institute (UPV/EHU, CSIC), University of the Basque Country, Leioa, Spain (A.B.-V., A.L.-S., U.G.-G., S.J.-B., C.M.).

Background: PCSK9 (Proprotein convertase subtilisin/kexin type 9) regulates LDL-C (low-density lipoprotein cholesterol) metabolism by targeting LDLr (LDL receptor) for lysosomal degradation. PCSK9 gain-of-function variants cause autosomal dominant hypercholesterolemia by reducing LDLr levels, the D374Y variant being the most severe, while loss-of-function variants are associated with low LDL-C levels. Gain-of-function and loss-of-function activities have also been attributed to variants occurring in the PCSK9 signal peptide. Read More

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Increased Capillary Permeability in Heart Induces Diastolic Dysfunction Independently of Inflammation, Fibrosis, or Cardiomyocyte Dysfunction.

Arterioscler Thromb Vasc Biol 2022 Jun 5;42(6):745-763. Epub 2022 May 5.

University of Bordeaux, INSERM, Biologie des maladies cardiovasculaires, U1034, Pessac, France (A.A., M.C., S.R., P.B., V.D., M.P., I.F., M.L.B., M.-A.R., P.D., T.C., C.D.).

Background: While endothelial dysfunction is suggested to contribute to heart failure with preserved ejection fraction pathophysiology, understanding the importance of the endothelium alone, in the pathogenesis of diastolic abnormalities has not yet been fully elucidated. Here, we investigated the consequences of specific endothelial dysfunction on cardiac function, independently of any comorbidity or risk factor (diabetes or obesity) and their potential effect on cardiomyocyte.

Methods: The ubiquitine ligase , expressed in endothelial cells (ECs), was shown to destabilize tight junction. Read More

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Perspectives on Cognitive Phenotypes and Models of Vascular Disease.

Arterioscler Thromb Vasc Biol 2022 Jul 5;42(7):831-838. Epub 2022 May 5.

Department of Cell and Developmental Biology, Northwestern University, Feinberg School of Medicine, Chicago, IL (M.L.I.-A.).

Clinical investigations have established that vascular-associated medical conditions are significant risk factors for various kinds of dementia. And yet, we are unable to associate certain types of vascular deficiencies with specific cognitive impairments. The reasons for this are many, not the least of which are that most vascular disorders are multi-factorial and the development of vascular dementia in humans is often a multi-year or multi-decade progression. Read More

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