9,374 results match your criteria Arterioscler. Thromb. Vasc. Biol.[Journal]


Comparison of Venous Thromboembolism Risks Between COVID-19 Pneumonia and Community-Acquired Pneumonia Patients.

Arterioscler Thromb Vasc Biol 2020 Jul 6:ATVBAHA120314779. Epub 2020 Jul 6.

Division of Vascular and Endovascular Surgery, Department of Surgery, University of Washington and Puget Sound VA Health Care System, Seattle (W.W.Z.).

Objective: The objectives were to investigate and compare the risks and incidences of venous thromboembolism (VTE) between the 2 groups of patients with coronavirus disease 2019 (COVID-19) pneumonia and community-acquired pneumonia (CAP). Approach and Results: Medical records of 616 pneumonia patients who were admitted to the Yichang Central People's Hospital in Hubei, China, from January 1 to March 23, 2020, were retrospectively reviewed. The patients with COVID-19 pneumonia were treated in the dedicated COVID-19 units, and the patients with CAP were admitted to regular hospital campus. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314779DOI Listing

Plant Stanol Esters Reduce LDL (Low-Density Lipoprotein) Aggregation by Altering LDL Surface Lipids: The BLOOD FLOW Randomized Intervention Study.

Arterioscler Thromb Vasc Biol 2020 Jul 2:ATVBAHA120314329. Epub 2020 Jul 2.

From the Atherosclerosis Research Laboratory, Wihuri Research Institute, Helsinki, Finland (M.R., L.A., F.T.-S., P.T.K., K.O.).

Objective: Plant stanol ester supplementation (2-3 g plant stanols/d) reduces plasma LDL (low-density lipoprotein) cholesterol concentration by 9% to 12% and is, therefore, recommended as part of prevention and treatment of atherosclerotic cardiovascular disease. In addition to plasma LDL-cholesterol concentration, also qualitative properties of LDL particles can influence atherogenesis. However, the effect of plant stanol ester consumption on the proatherogenic properties of LDL has not been studied. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314329DOI Listing

Gut Microbiota Restricts NETosis in Acute Mesenteric Ischemia-Reperfusion Injury.

Arterioscler Thromb Vasc Biol 2020 Jul 2:ATVBAHA120314491. Epub 2020 Jul 2.

From the Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University of Mainz (JGU), Germany (S.A., E.W., G.P., H.F., F.B., M.M., F.M., A.G., M.B., M.S., I.B., K.G., K.K., K.J., C.R.).

Objective: Recruitment of neutrophils and formation of neutrophil extracellular traps (NETs) contribute to lethality in acute mesenteric infarction. To study the impact of the gut microbiota in acute mesenteric infarction, we used gnotobiotic mouse models to study whether gut commensals prime the reactivity of neutrophils towards NETosis. Approach and Results: We applied a mesenteric ischemia-reperfusion (I/R) injury model to germ-free (GF) and colonized C57BL/6J mice. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314491DOI Listing

High Throughput Screen Identifies the DNMT1 (DNA Methyltransferase-1) Inhibitor, 5-Azacytidine, as a Potent Inducer of PTEN (Phosphatase and Tensin Homolog): Central Role for PTEN in 5-Azacytidine Protection Against Pathological Vascular Remodeling.

Arterioscler Thromb Vasc Biol 2020 Jun 25:ATVBAHA120314458. Epub 2020 Jun 25.

From the Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora. (K.A.S., S.L., M.F.M., A.J.J., A.M.D., R.A.N., M.C.M.W.-E.).

Objective: Our recent work demonstrates that PTEN (phosphatase and tensin homolog) is an important regulator of smooth muscle cell (SMC) phenotype. SMC-specific PTEN deletion promotes spontaneous vascular remodeling and PTEN loss correlates with increased atherosclerotic lesion severity in human coronary arteries. In mice, PTEN overexpression reduces plaque area and preserves SMC contractile protein expression in atherosclerosis and blunts Ang II (angiotensin II)-induced pathological vascular remodeling, suggesting that pharmacological PTEN upregulation could be a novel therapeutic approach to treat vascular disease. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314458DOI Listing

Role of PAR1-Egr1 in the Initiation of Thoracic Aortic Aneurysm in Fbln4-Deficient Mice.

Arterioscler Thromb Vasc Biol 2020 Jun 25:ATVBAHA120314560. Epub 2020 Jun 25.

From theLife Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Ibaraki, Japan. (S.J.S., H.T.H., T.S., Y.Y., H.Y.).

Objective: Remodeling of the extracellular matrix plays a vital role in cardiovascular diseases. Using a mouse model of postnatal ascending aortic aneurysms (termed ), we have reported that abnormal mechanosensing led to aneurysm formation in with an upregulation of the mechanosensitive transcription factor, Egr1 (Early growth response 1). However, the role of Egr1 and its upstream regulator(s) in the initiation of aneurysm development and their relationship to an aneurysmal microenvironment are unknown. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314560DOI Listing

Epidemiology and Risk of Amputation in Patients With Diabetes Mellitus and Peripheral Artery Disease.

Arterioscler Thromb Vasc Biol 2020 Jun 25:ATVBAHA120314595. Epub 2020 Jun 25.

From the Heart and Vascular Center, Dartmouth-Hitchcock Medical Center, Lebanon, NH.

Peripheral artery disease (PAD) stems from atherosclerosis of lower extremity arteries with resultant arterial narrowing or occlusion. The most severe form of PAD is termed chronic limb-threatening ischemia and carries a significant risk of limb loss and cardiovascular mortality. Diabetes mellitus is known to increase the incidence of PAD, accelerate disease progression, and increase disease severity. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314595DOI Listing

Loss-of-Function Variants in Patients With Severe Hypertriglyceridemia.

Arterioscler Thromb Vasc Biol 2020 Jun 25:ATVBAHA120314168. Epub 2020 Jun 25.

From the Robarts Research Institute, Western University, London, ON, Canada (J.S.D., A.A.D., A.L., A.D.M., J.W., H.C., R.A.H.).

Objective: Genetic determinants of severe hypertriglyceridemia include both common variants with small effects (assessed using polygenic risk scores) plus heterozygous and homozygous rare variants in canonical genes directly affecting triglyceride metabolism. Here, we broadened our scope to detect associations with rare loss-of-function variants in genes affecting noncanonical pathways, including those known to affect triglyceride metabolism indirectly. Approach and Results: From targeted next-generation sequencing of 69 metabolism-related genes in 265 patients of European descent with severe hypertriglyceridemia (≥10 mmol/L or ≥885 mg/dL) and 477 normolipidemic controls, we focused on the association of rare heterozygous loss-of-function variants in individual genes. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314168DOI Listing

VWF (von Willebrand Factor) Is Not Required for Red Blood Cell Retention in Clots in Mice.

Arterioscler Thromb Vasc Biol 2020 Jun 25:ATVBAHA120314575. Epub 2020 Jun 25.

From the Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill. (L.A.H., D.M.M., A.S.W.).

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http://dx.doi.org/10.1161/ATVBAHA.120.314575DOI Listing

Coronary Artery Disease.

Arterioscler Thromb Vasc Biol 2020 Jul 24;40(7):e185-e192. Epub 2020 Jun 24.

From the Center for the Study of Adversity and Cardiovascular Disease (NURTURE Center), Division of Cardiology, Department of Medicine, University of California San Francisco (H.A., M.A.A.).

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http://dx.doi.org/10.1161/ATVBAHA.120.313608DOI Listing

Effect of Weight Gain on Skeletal Muscle and Adipose Tissue Perfusion: Human Fat Goes With the Flow.

Arterioscler Thromb Vasc Biol 2020 Jul 24;40(7):1617-1619. Epub 2020 Jun 24.

Department of Cardiovascular Medicine, University of Massachusetts Medical School, Worcester.

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http://dx.doi.org/10.1161/ATVBAHA.120.314663DOI Listing

Platelets and Immunity: Going Viral.

Arterioscler Thromb Vasc Biol 2020 07 24;40(7):1605-1607. Epub 2020 Jun 24.

From the Department of Medicine, University of Massachusetts Medical School, Worcester.

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http://dx.doi.org/10.1161/ATVBAHA.120.314620DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7319043PMC

Reining in Peripheral Arterial Calcification.

Arterioscler Thromb Vasc Biol 2020 Jul 24;40(7):1614-1616. Epub 2020 Jun 24.

From the Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor.

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http://dx.doi.org/10.1161/ATVBAHA.120.314665DOI Listing

Soothing a Broken Heart: Can Therapeutic Cross-Talk Between Lymphatics and the Immune Response Improve Recovery From Myocardial Infarction?

Arterioscler Thromb Vasc Biol 2020 Jul 24;40(7):1611-1613. Epub 2020 Jun 24.

From the Tumour Angiogenesis and Microenvironment Program, Peter MacCallum Cancer Centre (R.H.F., S.A.S.), Victoria, Australia.

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http://dx.doi.org/10.1161/ATVBAHA.120.314666DOI Listing

SR-BI (Scavenger Receptor BI), Not LDL (Low-Density Lipoprotein) Receptor, Mediates Adrenal Stress Response.

Arterioscler Thromb Vasc Biol 2020 Jun 11:ATVBAHA120314506. Epub 2020 Jun 11.

From the Saha Cardiovascular Research Center, University of Kentucky College of Medicine, Lexington. (M.I., X.Y., Q.W., L.G., D. Hao, D. Howatt, A.D., L.C., R.T., X.-A.L.).

Objective: Adrenal gland secretes stress-induced glucocorticoids (iGCs) to coping with stress. Previous study showed that SR-BI (scavenger receptor BI) null (SR-BI) mice failed to generate iGC in stress conditions, suggesting that SR-BI-mediated cholesterol uptake from HDL (high-density lipoprotein) is a key regulator for iGC production. However, the LDL (low-density lipoprotein)/LDLr (LDL receptor) pathway can also provide cholesterol for iGC synthesis, but rodents have limited LDL levels in circulation. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314506DOI Listing
June 2020
6.000 Impact Factor

ADAM (a Disintegrin and Metalloproteinase) 15 Deficiency Exacerbates Ang II (Angiotensin II)-Induced Aortic Remodeling Leading to Abdominal Aortic Aneurysm.

Arterioscler Thromb Vasc Biol 2020 Jun 11:ATVBAHA120314600. Epub 2020 Jun 11.

From the Department of Physiology, Cardiovascular Research Center, University of Alberta, Edmonton, Canada (S.J., M.C., M.H., G.Y.O., Z.K.).

Objective: ADAM (a disintegrin and metalloproteinase) 15-a membrane-bound metalloprotease from the ADAM (disintegrin and metalloproteinase) family-has been linked to endothelial permeability, inflammation, and metastasis. However, its function in aortic aneurysm has not been explored. We aimed to determine the function of ADAM15 in the pathogenesis of aortic remodeling and aneurysm formation. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314600DOI Listing
June 2020
6.000 Impact Factor

Overcoming Barriers: The Endothelium As a Linchpin of Coronavirus Disease 2019 Pathogenesis?

Arterioscler Thromb Vasc Biol 2020 Jun 8:ATVBAHA120314558. Epub 2020 Jun 8.

From the Toronto General Hospital Research Institute, University Health Network, Canada (D.G., S.R., R.W., C.C., S.V., K.R., E.B., K.L.H., J.E.F.).

Objective: Coronavirus disease 2019 (COVID-19) is a global pandemic involving >5 500 000 cases worldwide as of May 26, 2020. The culprit is the severe acute respiratory syndrome coronavirus-2, which invades cells by binding to angiotensin-converting enzyme 2. While the majority of patients mount an appropriate antiviral response and recover at home, others progress to respiratory distress requiring hospital admission for supplemental oxygen. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314558DOI Listing

Novel Mouse Model for Studying Hemostatic Function of Human Platelets.

Arterioscler Thromb Vasc Biol 2020 Jun 4:ATVBAHA120314304. Epub 2020 Jun 4.

From the Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill (D.S.P., W.B.).

Objective: Platelets are critical to the formation of a hemostatic plug and the pathogenesis of atherothrombosis. Preclinical animal models, especially the mouse, provide an important platform to assess the efficacy and safety of antiplatelet drugs. However, these studies are limited by inherent differences between human and mouse platelets and the species-selectivity of many drugs. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314304DOI Listing

Macrophage (Drp1) Dynamin-Related Protein 1 Accelerates Intimal Thickening After Vascular Injury.

Arterioscler Thromb Vasc Biol 2020 Jun 4:ATVBAHA120314383. Epub 2020 Jun 4.

the Department of Cardiovascular Research, Development, and Translational Medicine, Center for Cardiovascular Disruptive Innovation, Kyushu University, Fukuoka, Japan (J.K., K.E.).

Objective: Mitochondria consistently change their morphology in a process regulated by proteins, including Drp1 (dynamin-related protein 1), a protein promoting mitochondrial fission. Drp1 is involved in the mechanisms underlying various cardiovascular diseases, such as myocardial ischemia/reperfusion injury, heart failure, and pulmonary arterial hypertension. However, its role in macrophages, which promote various vascular diseases, is poorly understood. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314383DOI Listing

Serum Calcification Propensity and the Risk of Cardiovascular and All-Cause Mortality in the General Population: The PREVEND Study.

Arterioscler Thromb Vasc Biol 2020 Jun 4:ATVBAHA120314187. Epub 2020 Jun 4.

From the Division of Nephrology, University of Groningen, University Medical Center Groningen, The Netherlands (C.E., C.A.t.V.-K., R.T.G., S.J.L.B., M.H.d.B.).

Objective: Vascular calcification contributes to the cause of cardiovascular disease. The calciprotein particle maturation time (T) in serum, a measure of calcification propensity, has been linked with adverse outcomes in patients with chronic kidney disease, but its role in the general population is unclear. We investigated whether serum T is associated with cardiovascular mortality in a large general population-based cohort. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314187DOI Listing

Mature Vascular Smooth Muscle Cells, but Not Endothelial Cells, Serve as the Major Cellular Source of Intimal Hyperplasia in Vein Grafts.

Arterioscler Thromb Vasc Biol 2020 Jun 4:ATVBAHA120314465. Epub 2020 Jun 4.

From the Department of Cell Biology and Anatomy, University of South Carolina, Columbia, SC (W.W., C.W., H.Z., L.Q., M.A., T.C.).

Objective: Neointima formation is a primary cause of intermediate to late vein graft (VG) failure. However, the precise source of neointima cells in VGs remains unclear. Approach and Results: Herein we clarify the relative contributions of mature vascular smooth muscle cells (SMCs) and endothelial cells (ECs) to neointima formation in a mouse model of VG remodeling via the genetic-inducible fate mapping approaches. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314465DOI Listing

DDR1 (Discoidin Domain Receptor-1)-RhoA (Ras Homolog Family Member A) Axis Senses Matrix Stiffness to Promote Vascular Calcification.

Arterioscler Thromb Vasc Biol 2020 Jul 4;40(7):1763-1776. Epub 2020 Jun 4.

From the Department of Laboratory Medicine and Pathobiology (D.N., M.L., M.P.B.), University of Toronto, Canada.

Objective: Vascular calcification is a pathology characterized by arterial mineralization, which is a common late-term complication of atherosclerosis that independently increases the risk of adverse cardiovascular events by fourfold. A major source of calcifying cells is transdifferentiating vascular smooth muscle cells (VSMCs). Previous studies showed that deletion of the collagen-binding receptor, DDR1 (discoidin domain receptor-1), attenuated VSMC calcification. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314697DOI Listing

S100A9-RAGE Axis Accelerates Formation of Macrophage-Mediated Extracellular Vesicle Microcalcification in Diabetes Mellitus.

Arterioscler Thromb Vasc Biol 2020 May 28:ATVBAHA118314087. Epub 2020 May 28.

From the Center for Excellence in Vascular Biology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (R.K., S.K., R.T., D.C.R., D.B.-G., L.S.A.P., G.K.S., P.L., M.A., K.C., E.A.).

Objective: Vascular calcification is a cardiovascular risk factor and accelerated in diabetes mellitus. Previous work has established a role for calcification-prone extracellular vesicles in promoting vascular calcification. However, the mechanisms by which diabetes mellitus provokes cardiovascular events remain incompletely understood. Read More

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http://dx.doi.org/10.1161/ATVBAHA.118.314087DOI Listing

TGFβ (Transforming Growth Factor-Beta)-Activated Kinase 1 Regulates Arteriovenous Fistula Maturation.

Arterioscler Thromb Vasc Biol 2020 Jul 28;40(7):e203-e213. Epub 2020 May 28.

Department of Surgery (H.H., S.-R.L., H.B., J.G., T.H., T.I., X.G., T.W., K.W., S.L., S.O., B.Y., A.D.), Yale University School of Medicine, New Haven, CT.

Objective: Arteriovenous fistulae (AVF) are the optimal conduit for hemodialysis access but have high rates of primary maturation failure. Successful AVF maturation requires wall thickening with deposition of ECM (extracellular matrix) including collagen and fibronectin, as well as lumen dilation. TAK1 (TGFβ [transforming growth factor-beta]-activated kinase 1) is a mediator of noncanonical TGFβ signaling and plays crucial roles in regulation of ECM production and deposition; therefore, we hypothesized that TAK1 regulates wall thickening and lumen dilation during AVF maturation. Read More

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http://dx.doi.org/10.1161/ATVBAHA.119.313848DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7316601PMC
July 2020
6.000 Impact Factor

Sex-Specific Regulation of Inflammation and Metabolic Syndrome in Obesity.

Arterioscler Thromb Vasc Biol 2020 Jul 28;40(7):1787-1800. Epub 2020 May 28.

From the Department of Internal Medicine and Radboud Institute for Molecular Life Sciences (R.t.H., I.C.L.v.d.M., K.S., M.J., S.P.S., T.B., H.L., H.D., J.d.G., L.A.B.J., J.H.W.R., M.G.N., N.P.R.), Radboud University Medical Center, Nijmegen, the Netherlands.

Objective: Metabolic dysregulation and inflammation are important consequences of obesity and impact susceptibility to cardiovascular disease. Anti-inflammatory therapy in cardiovascular disease is being developed under the assumption that inflammatory pathways are identical in women and men, but it is not known if this is indeed the case. In this study, we assessed the sex-specific relation between inflammation and metabolic dysregulation in obesity. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314508DOI Listing

Global Plasma Metabolomics to Identify Potential Biomarkers of Blood Pressure Progression.

Arterioscler Thromb Vasc Biol 2020 May 28:ATVBAHA120314356. Epub 2020 May 28.

From the Department of Medical Sciences, Uppsala University, Sweden (Y.-T.L., S.S., T.F., U.H., E.I., L.L., J.S.).

Objective: The pathophysiology of hypertension remains incompletely understood. We investigated associations of circulating metabolites with longitudinal blood pressure (BP) changes in the Prospective Investigation of the Vasculature in Uppsala Seniors cohort and validated the findings in the Uppsala Longitudinal Study of Adult Men cohort. Approach and Results: Circulating metabolite levels were assessed with liquid- and gas-chromatography coupled to mass spectrometry among persons without BP-lowering medication at baseline. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314356DOI Listing

Association of TIM-1 (T-Cell Immunoglobulin and Mucin Domain 1) With Incidence of Stroke.

Arterioscler Thromb Vasc Biol 2020 Jul 28;40(7):1777-1786. Epub 2020 May 28.

Department of Clinical Sciences, Lund University, Malmö, Sweden (J.S., M.S., O.M., M.O.-M., J.N., Y.B., G.E.).

Objective: The aim of this study was to investigate if there is a causal relationship between circulating levels of TIM-1 (T-cell immunoglobulin and mucin domain 1) and incidence of stroke. Approach and Results: Plasma TIM-1 was analyzed in 4591 subjects (40% men; mean age, 57.5 years) attending the Malmö Diet and Cancer Study. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314269DOI Listing

Correction to: MiR-15b-5p Regulates Collateral Artery Formation by Targeting AKT3 (Protein Kinase B-3).

Authors:

Arterioscler Thromb Vasc Biol 2020 06 27;40(6):e183. Epub 2020 May 27.

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http://dx.doi.org/10.1161/ATV.0000000000000110DOI Listing

Vascular Endothelial Cells and Innate Immunity.

Arterioscler Thromb Vasc Biol 2020 06 27;40(6):e138-e152. Epub 2020 May 27.

From the Centers of Inflammation, Translational, and Clinical Lung Research (Y. Shao, Y. Sun, Y.L., F.S., C.D., C.J., K.X., X.J., X.Y.), Temple University, Lewis Katz School of Medicine, Philadelphia, PA.

In addition to the roles of endothelial cells (ECs) in physiological processes, ECs actively participate in both innate and adaptive immune responses. We previously reported that, in comparison to macrophages, a prototypic innate immune cell type, ECs have many innate immune functions that macrophages carry out, including cytokine secretion, phagocytic function, antigen presentation, pathogen-associated molecular patterns-, and danger-associated molecular patterns-sensing, proinflammatory, immune-enhancing, anti-inflammatory, immunosuppression, migration, heterogeneity, and plasticity. In this highlight, we introduce recent advances published in both and many other journals: (1) several significant characters classify ECs as novel immune cells not only in infections and allograft transplantation but also in metabolic diseases; (2) several new receptor systems including conditional danger-associated molecular pattern receptors, nonpattern receptors, and homeostasis associated molecular patterns receptors contribute to innate immune functions of ECs; (3) immunometabolism and innate immune memory determine the innate immune functions of ECs; (4) a great induction of the immune checkpoint receptors in ECs during inflammations suggests the immune tolerogenic functions of ECs; and (5) association of immune checkpoint inhibitors with cardiovascular adverse events and cardio-oncology indicates the potential contributions of ECs as innate immune cells. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314330DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7263359PMC
June 2020
6.000 Impact Factor

Response by Goody and Jansen to Letter Regarding Article, "Aortic Valve Stenosis: From Basic Mechanisms to Novel Therapeutic Targets".

Arterioscler Thromb Vasc Biol 2020 06 27;40(6):e182. Epub 2020 May 27.

From the Department of Medicine II, Heart Center Bonn, University Hospital Bonn, Germany.

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http://dx.doi.org/10.1161/ATVBAHA.120.314464DOI Listing

Letter by Tziakas et al Regarding Article, "Aortic Valve Stenosis: From Basic Mechanisms to Novel Therapeutic Targets".

Arterioscler Thromb Vasc Biol 2020 06 27;40(6):e180-e181. Epub 2020 May 27.

Center for Cardiology, Cardiology I (K.S.), University Medical Center of the Johannes Gutenberg University Mainz, German.

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http://dx.doi.org/10.1161/ATVBAHA.120.314456DOI Listing

IL-1R (Interleukin-1 Receptor) Signaling and Attenuated Hepatic CYP (Cytochrome P450) 2C Expression: Explanation for Higher Rate of Clopidogrel Resistance in Patients With Diabetes Mellitus?

Authors:
Rolf P Kreutz

Arterioscler Thromb Vasc Biol 2020 06 27;40(6):1429-1431. Epub 2020 May 27.

From the Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis.

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http://dx.doi.org/10.1161/ATVBAHA.120.314446DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7263358PMC

Differential Roles of Endothelial Cell-Derived and Smooth Muscle Cell-Derived Fibronectin Containing Extra Domain A in Early and Late Atherosclerosis.

Arterioscler Thromb Vasc Biol 2020 Jul 21;40(7):1738-1747. Epub 2020 May 21.

From the Division of Hematology/Oncology, Department of Internal Medicine, University of Iowa, Iowa City.

Objective: The extracellular matrix of atherosclerotic arteries contains abundant deposits of cellular Fn-EDA (fibronectin containing extra domain A), suggesting a functional role in the pathophysiology of atherosclerosis. Fn-EDA is synthesized by several cell types, including endothelial cells (ECs) and smooth muscle cells (SMCs), which are known to contribute to different stages of atherosclerosis. Although previous studies using global Fn-EDA-deficient mice have demonstrated that Fn-EDA is proatherogenic, the cell-specific role of EC versus SMC-derived-Fn-EDA in atherosclerosis has not been investigated yet. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314459DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7337357PMC
July 2020
6.000 Impact Factor

Platelets Endocytose Viral Particles and Are Activated via TLR (Toll-Like Receptor) Signaling.

Arterioscler Thromb Vasc Biol 2020 Jul 21;40(7):1635-1650. Epub 2020 May 21.

Department of Molecular and Cellular Biochemistry (M.B., S.J., G.J.P., M.D.M., S.W.W.), University of Kentucky, Lexington.

Objective: Thrombocytopenia is associated with many viral infections suggesting virions interact with and affect platelets. Consistently, viral particles are seen inside platelets, and platelet activation markers are detected in viremic patients. In this article, we sought mechanistic insights into these virion/platelet interactions by examining how platelets endocytose, traffic, and are activated by a model virion. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314180DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7316618PMC

TDAG51 (T-Cell Death-Associated Gene 51) Is a Key Modulator of Vascular Calcification and Osteogenic Transdifferentiation of Arterial Smooth Muscle Cells.

Arterioscler Thromb Vasc Biol 2020 Jul 21;40(7):1664-1679. Epub 2020 May 21.

From the Division of Nephrology, Department of Medicine (K.P., P.F.L., G.G., Š.L., M.E.M., G.P., J.H.B., A.J.I., J.C.K., R.C.A.), McMaster University, and The Research Institute of St. Joseph's Hamilton, ON, Canada.

Objective: Cardiovascular disease is the primary cause of mortality in patients with chronic kidney disease. Vascular calcification (VC) in the medial layer of the vessel wall is a unique and prominent feature in patients with advanced chronic kidney disease and is now recognized as an important predictor and independent risk factor for cardiovascular and all-cause mortality in these patients. VC in chronic kidney disease is triggered by the transformation of vascular smooth muscle cells (VSMCs) into osteoblasts as a consequence of elevated circulating inorganic phosphate (P) levels, due to poor kidney function. Read More

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http://dx.doi.org/10.1161/ATVBAHA.119.313779DOI Listing
July 2020
6.000 Impact Factor

Vascular Regeneration in Peripheral Artery Disease.

Arterioscler Thromb Vasc Biol 2020 Jul 21;40(7):1627-1634. Epub 2020 May 21.

From the Department of Cardiovascular Sciences, Center for Cardiovascular Regeneration, Houston Methodist Research Institute, TX.

Peripheral artery disease is a common disorder and a major cause of morbidity and mortality worldwide. Therapy is directed at reducing the risk of major adverse cardiovascular events and at ameliorating symptoms. Medical therapy is effective at reducing the incidence of myocardial infarction and stroke to which these patients are prone but is inadequate in relieving limb-related symptoms, such as intermittent claudication, rest pain, and ischemic ulceration. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.312862DOI Listing

Effects of a Hypercaloric and Hypocaloric Diet on Insulin-Induced Microvascular Recruitment, Glucose Uptake, and Lipolysis in Healthy Lean Men.

Arterioscler Thromb Vasc Biol 2020 Jul 14;40(7):1695-1704. Epub 2020 May 14.

From the Department of Internal Medicine (A.L.E., R.I.M., J.W., D.H.v.R., M.D., M.H.H.K., E.H.S.), Amsterdam UMC, location VU University Medical Center, Amsterdam Cardiovascular Sciences, Amsterdam, The Netherlands.

Objective: In mice fed a high-fat diet, impairment of insulin signaling in endothelium is an early phenomenon that precedes decreased insulin sensitivity of skeletal muscle, adipose tissue, and liver. We assessed in humans whether short-term overfeeding affects insulin-induced microvascular recruitment in skeletal muscle and adipose tissue before changes occur in glucose uptake and lipolysis. Approach and Results: Fifteen healthy males underwent a hypercaloric and subsequent hypocaloric diet intervention. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314129DOI Listing

Lymphatic and Immune Cell Cross-Talk Regulates Cardiac Recovery After Experimental Myocardial Infarction.

Arterioscler Thromb Vasc Biol 2020 Jul 14;40(7):1722-1737. Epub 2020 May 14.

From the Normandy University, UniRouen, Inserm (Institut National de la Santé et de la Recherche Médicale) UMR1096 (EnVI Laboratory), FHU REMOD-VHF, Rouen, France (H.M., A.D., V.T., I.B., J.P.H., S.R., J.R., S.F., V.R., P.M.).

Objective: Lymphatics play an essential pathophysiological role in promoting fluid and immune cell tissue clearance. Conversely, immune cells may influence lymphatic function and remodeling. Recently, cardiac lymphangiogenesis has been proposed as a therapeutic target to prevent heart failure after myocardial infarction (MI). Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314370DOI Listing
July 2020
6.000 Impact Factor

In Vitro Lineage-Specific Differentiation of Vascular Smooth Muscle Cells in Response to SMAD3 Deficiency: Implications for SMAD3-Related Thoracic Aortic Aneurysm.

Arterioscler Thromb Vasc Biol 2020 Jul 14;40(7):1651-1663. Epub 2020 May 14.

From the Department of Cardiac Surgery, North Campus Research Complex, University of Michigan, Ann Arbor (J.G., D.Z., L.J., P.Q., Y.E.C., B.Y.).

Objective: SMAD3 pathogenic variants are associated with the development of thoracic aortic aneurysms. We sought to determine the role of SMAD3 in lineage-specific vascular smooth muscle cells (VSMCs) differentiation and function. Approach and Results: c. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.313033DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7316596PMC

DNA Damage Response: A Molecular Lynchpin in the Pathobiology of Arteriosclerotic Calcification.

Arterioscler Thromb Vasc Biol 2020 Jul 14;40(7):e193-e202. Epub 2020 May 14.

British Heart Foundation Centre of Research Excellence, School of Cardiovascular Medicine and Sciences, King's College London, United Kingdom (A.M.C., C.M.S.).

Vascular calcification is a ubiquitous pathology of aging. Oxidative stress, persistent DNA damage, and senescence are major pathways driving both cellular and tissue aging, and emerging evidence suggests that these pathways are activated, and even accelerated, in patients with vascular calcification. The DNA damage response-a complex signaling platform that maintains genomic integrity-is induced by oxidative stress and is intimately involved in regulating cell death and osteogenic differentiation in both bone and the vasculature. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.313792DOI Listing

PKC (Protein Kinase C)-δ Modulates AT (Antithrombin) Signaling in Vascular Endothelial Cells.

Arterioscler Thromb Vasc Biol 2020 Jul 14;40(7):1748-1762. Epub 2020 May 14.

From the Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation (S.R.P., I.B., H.G., X.C., A.R.R.).

Objective: Native and latent conformers of AT (antithrombin) induce anti-inflammatory and proapoptotic signaling activities, respectively, in vascular endothelial cells by unknown mechanisms. Synd-4 (syndecan-4) has been identified as a receptor that is involved in transmitting signaling activities of AT in endothelial cells. Approach and Results: In this study, we used flow cytometry, signaling assays, immunoblotting and confocal immunofluorescence microscopy to investigate the mechanism of the paradoxical signaling activities of high-affinity heparin (native) and low-affinity heparin (latent) conformers of AT in endothelial cells. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314479DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7316612PMC
July 2020
6.000 Impact Factor

Orchestration of Primary Hemostasis by Platelet and Endothelial Lysosome-Related Organelles.

Arterioscler Thromb Vasc Biol 2020 06 7;40(6):1441-1453. Epub 2020 May 7.

From the Department of Molecular and Cellular Hemostasis, Sanquin Research and Landsteiner Laboratory (E.K., R.B., J.V.), Amsterdam University Medical Center, University of Amsterdam, the Netherlands.

Megakaryocyte-derived platelets and endothelial cells store their hemostatic cargo in α- and δ-granules and Weibel-Palade bodies, respectively. These storage granules belong to the lysosome-related organelles (LROs), a heterogeneous group of organelles that are rapidly released following agonist-induced triggering of intracellular signaling pathways. Following vascular injury, endothelial Weibel-Palade bodies release their content into the vascular lumen and promote the formation of long VWF (von Willebrand factor) strings that form an adhesive platform for platelets. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314245DOI Listing

Dysregulation of FOXO1 (Forkhead Box O1 Protein) Drives Calcification in Arterial Calcification due to Deficiency of CD73 and Is Present in Peripheral Artery Disease.

Arterioscler Thromb Vasc Biol 2020 Jul 7;40(7):1680-1694. Epub 2020 May 7.

From the Department of Medicine, Division of Cardiology, University of Pittsburgh, PA (W.J.M., C.C.C., R.A.C., J.C., R.W., C.R., C.K.B., S.S., M.L., D.G., C.S.H.).

Objective: The recessive disease arterial calcification due to deficiency of CD73 (ACDC) presents with extensive nonatherosclerotic medial layer calcification in lower extremity arteries. Lack of CD73 induces a concomitant increase in TNAP (tissue nonspecific alkaline phosphatase; ), a key enzyme in ectopic mineralization. Our aim was to investigate how loss of CD73 activity leads to increased expression and calcification in CD73-deficient patients and assess whether this mechanism may apply to peripheral artery disease calcification. Read More

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http://dx.doi.org/10.1161/ATVBAHA.119.313765DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7310306PMC

F-Sodium Fluoride (F-NaF) for Imaging Microcalcification Activity in the Cardiovascular System.

Arterioscler Thromb Vasc Biol 2020 Jul 7;40(7):1620-1626. Epub 2020 May 7.

From the BHF Centre for Cardiovascular Science, University of Edinburgh, United Kingdom.

Accumulating preclinical and clinical evidence suggests that calcification is one of the body's primary responses to injury and a key pathological feature of cardiovascular disease. Calcification activity can now be imaged using F-sodium fluoride (F-NaF) positron emission tomography (PET) in combination with either computed tomography or magnetic resonance. These techniques allow visualization of calcification activity and, therefore, provide different information to the established macroscopic calcium imaged with computed tomography. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.313785DOI Listing

Cav-1 (Caveolin-1) Deficiency Increases Autophagy in the Endothelium and Attenuates Vascular Inflammation and Atherosclerosis.

Arterioscler Thromb Vasc Biol 2020 06 30;40(6):1510-1522. Epub 2020 Apr 30.

From the Vascular Biology and Therapeutics Program (X.Z., C.M.R., B.A., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.

Objective: Endothelial Cav-1 (caveolin-1) expression plays a relevant role during atherogenesis by controlling NO production, vascular inflammation, LDL (low-density lipoprotein) transcytosis, and extracellular matrix remodeling. Additional studies have identified cholesterol-rich membrane domains as important regulators of autophagy by recruiting ATGs (autophagy-related proteins) to the plasma membrane. Here, we investigate how the expression of Cav-1 in the aortic endothelium influences autophagy and whether enhanced autophagy contributes to the atheroprotective phenotype observed in Cav-1-deficient mice. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314291DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253189PMC

sLRP1 (Soluble Low-Density Lipoprotein Receptor-Related Protein 1): A Novel Biomarker for P2Y12 (P2Y Purinoceptor 12) Receptor Expression in Atherosclerotic Plaques.

Arterioscler Thromb Vasc Biol 2020 06 30;40(6):e166-e179. Epub 2020 Apr 30.

From the Department of Neurology (J.C., S.P., H.S., Y. Liu, X.G., L.Z., Y. Li, H.H., Y.X., L.M., B.H.), Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Objective: Recent studies suggest that the P2Y12 (P2Y purinoceptor 12) receptor of vascular smooth muscle cells in atherosclerotic plaques aggravates atherosclerosis, and P2Y12 receptor inhibitors such as CDL (clopidogrel) may effectively treat atherosclerosis. It is imperative to identify an effective biomarker for reflecting the P2Y12 receptor expression on vascular smooth muscle cells in plaques. Approach and Results: We found that there was a positive correlation between the level of circulating sLRP1 (soluble low-density lipoprotein receptor-related protein 1) and the number of LRP1 α-SMA (α-smooth muscle actin), P2Y12, or P2Y12 LRP1 cells in plaques from apoE mice fed a high-fat diet. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314350DOI Listing

Bmal1 Deletion in Myeloid Cells Attenuates Atherosclerotic Lesion Development and Restrains Abdominal Aortic Aneurysm Formation in Hyperlipidemic Mice.

Arterioscler Thromb Vasc Biol 2020 06 23;40(6):1523-1532. Epub 2020 Apr 23.

The Institute for Translational Medicine and Therapeutics (S.Y.T., G.A.F.), University of Pennsylvania, Philadelphia.

Objective: Although the molecular components of circadian rhythms oscillate in discrete cellular components of the vasculature and many aspects of vascular function display diurnal variation, the cellular connections between the molecular clock and inflammatory cardiovascular diseases remain to be elucidated. Previously we have shown that pre- versus postnatal deletion of Bmal1 (brain and muscle aryl hydrocarbon receptor nuclear translocator-like 1), the nonredundant core clock gene has contrasting effects on atherogenesis. Here we investigated the effect of myeloid cell Bmal1 deletion on atherogenesis and abdominal aortic aneurysm formation in mice. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314318DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285859PMC

Excessive EP4 Signaling in Smooth Muscle Cells Induces Abdominal Aortic Aneurysm by Amplifying Inflammation.

Arterioscler Thromb Vasc Biol 2020 06 23;40(6):1559-1573. Epub 2020 Apr 23.

From the Cardiovascular Research Institute (T.H., U.Y., A.M., R.I., Y.I., M.U., T.F., Y.I.), Yokohama City University, Japan.

Objective: Excessive prostaglandin E production is a hallmark of abdominal aortic aneurysm (AAA). Enhanced expression of prostaglandin E receptor EP4 (prostaglandin E receptor 4) in vascular smooth muscle cells (VSMCs) has been demonstrated in human AAAs. Although moderate expression of EP4 contributes to vascular homeostasis, the roles of excessive EP4 in vascular pathology remain uncertain. Read More

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http://dx.doi.org/10.1161/ATVBAHA.120.314297DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253191PMC
June 2020
6.000 Impact Factor

Arteriosclerosis: A Primer for "In Focus" Reviews on Arterial Stiffness.

Arterioscler Thromb Vasc Biol 2020 05 22;40(5):1025-1027. Epub 2020 Apr 22.

Faculty of Medicine, Department of Surgery & Cancer, Imperial College London, United Kingdom (J.T.P.).

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http://dx.doi.org/10.1161/ATVBAHA.120.314208DOI Listing