Subjects -> MEDICAL SCIENCES (Total: 8185 journals)
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HEMATOLOGY (160 journals)                     

Showing 1 - 151 of 151 Journals sorted alphabetically
Acta Angiologica     Open Access   (Followers: 2)
Acta Haematologica     Full-text available via subscription   (Followers: 23)
Acta Haematologica Polonica     Open Access  
Adipocyte     Open Access  
Advances in Hematology     Open Access   (Followers: 13)
Africa Sanguine     Full-text available via subscription  
American Journal of Hematology     Hybrid Journal   (Followers: 52)
Anemia     Open Access   (Followers: 6)
Annals of Hematology     Hybrid Journal   (Followers: 15)
Archives of Hematology Case Reports and Reviews     Open Access  
Arteriosclerosis, Thrombosis and Vascular Biology     Full-text available via subscription   (Followers: 29)
Artery Research     Hybrid Journal   (Followers: 4)
Artificial Cells, Nanomedicine and Biotechnology     Hybrid Journal   (Followers: 4)
ASAIO Journal     Hybrid Journal   (Followers: 2)
Best Practice & Research Clinical Haematology     Hybrid Journal   (Followers: 5)
Blood     Hybrid Journal   (Followers: 296)
Blood Advances     Open Access   (Followers: 7)
Blood and Lymphatic Cancer : Targets and Therapy     Open Access   (Followers: 7)
Blood Cancer Journal     Open Access   (Followers: 18)
Blood Cells, Molecules, and Diseases     Hybrid Journal   (Followers: 8)
Blood Coagulation & Fibrinolysis     Hybrid Journal   (Followers: 60)
Blood Pressure     Open Access  
Blood Pressure Monitoring     Hybrid Journal   (Followers: 1)
Blood Purification     Full-text available via subscription   (Followers: 6)
Blood Reviews     Hybrid Journal   (Followers: 26)
BMC Hematology     Open Access   (Followers: 7)
BMJ Open Diabetes Research & Care     Open Access   (Followers: 29)
Bone Marrow Transplantation     Hybrid Journal   (Followers: 17)
British Journal of Diabetes & Vascular Disease     Open Access   (Followers: 21)
British Journal of Haematology     Hybrid Journal   (Followers: 60)
British Journal of Primary Care Nursing - Cardiovascular Disease, Diabetes and Kidney Care     Full-text available via subscription   (Followers: 10)
Canadian Journal of Diabetes     Hybrid Journal   (Followers: 28)
Case Reports in Hematology     Open Access   (Followers: 10)
Clinical and Applied Thrombosis/Hemostasis     Open Access   (Followers: 32)
Clinical Diabetes     Full-text available via subscription   (Followers: 39)
Clinical Diabetes and Endocrinology     Open Access   (Followers: 20)
Clinical Lymphoma & Myeloma     Full-text available via subscription   (Followers: 2)
Clinical Lymphoma Myeloma and Leukemia     Hybrid Journal   (Followers: 5)
Clinical Medicine Insights : Blood Disorders     Open Access   (Followers: 1)
Conquest : The Official Journal of Diabetes Australia     Full-text available via subscription   (Followers: 3)
Current Angiogenesis     Hybrid Journal   (Followers: 1)
Current Diabetes Reports     Hybrid Journal   (Followers: 24)
Current Diabetes Reviews     Hybrid Journal   (Followers: 27)
Current Hematologic Malignancy Reports     Hybrid Journal   (Followers: 2)
Current Opinion in Hematology     Hybrid Journal   (Followers: 20)
Cytotherapy     Full-text available via subscription   (Followers: 2)
Der Diabetologe     Hybrid Journal   (Followers: 2)
Diabetes     Full-text available via subscription   (Followers: 410)
Diabetes aktuell     Hybrid Journal   (Followers: 3)
Diabetes and Vascular Disease Research     Hybrid Journal   (Followers: 20)
Diabetes Care     Full-text available via subscription   (Followers: 469)
Diabetes Case Reports     Open Access  
Diabetes Educator     Hybrid Journal   (Followers: 27)
Diabetes Management     Full-text available via subscription   (Followers: 15)
Diabetes Research and Clinical Practice     Hybrid Journal   (Followers: 70)
Diabetes Spectrum     Full-text available via subscription   (Followers: 16)
Diabetes Technology & Therapeutics     Hybrid Journal   (Followers: 50)
Diabetes Therapy     Open Access   (Followers: 23)
Diabetic Foot & Ankle     Open Access   (Followers: 10)
Diabetic Medicine     Hybrid Journal   (Followers: 147)
Diabetologia     Hybrid Journal   (Followers: 205)
Diabetologia Kliniczna     Hybrid Journal  
Diabetologie und Stoffwechsel     Hybrid Journal   (Followers: 2)
Egyptian Journal of Haematology     Open Access  
eJHaem     Open Access  
European Journal of Haematology     Hybrid Journal   (Followers: 16)
Experimental Hematology     Hybrid Journal   (Followers: 6)
Experimental Hematology & Oncology     Open Access   (Followers: 6)
Expert Review of Hematology     Hybrid Journal   (Followers: 5)
Fluids and Barriers of the CNS     Open Access   (Followers: 1)
Global Journal of Transfusion Medicine     Open Access   (Followers: 1)
Haematologica - the Hematology journal     Open Access   (Followers: 33)
Haemophilia     Hybrid Journal   (Followers: 66)
Hematologia     Full-text available via subscription   (Followers: 3)
Hematología     Open Access  
Hematology     Open Access   (Followers: 15)
Hematology Reports     Open Access   (Followers: 4)
Hematology, Transfusion and Cell Therapy     Open Access   (Followers: 2)
Hematology/Oncology and Stem Cell Therapy     Open Access   (Followers: 6)
Hemodialysis International     Hybrid Journal   (Followers: 3)
Hepatitis Monthly     Open Access   (Followers: 3)
Immunohematology : Journal of Blood Group Serology and Molecular Genetics     Hybrid Journal   (Followers: 1)
Indian Journal of Hematology and Blood Transfusion     Hybrid Journal   (Followers: 2)
Info Diabetologie     Full-text available via subscription   (Followers: 1)
InFo Hämatologie + Onkologie : Interdisziplinäre Fortbildung von Ärzten für Ärzte     Full-text available via subscription  
Integrated Blood Pressure Control     Open Access  
International Blood Research & Reviews     Open Access  
International Journal of Clinical Transfusion Medicine     Open Access   (Followers: 3)
International Journal of Diabetes in Developing Countries     Hybrid Journal   (Followers: 6)
International Journal of Diabetes Research     Open Access   (Followers: 8)
International Journal of Hematologic Oncology     Open Access   (Followers: 2)
International Journal of Hematology     Hybrid Journal   (Followers: 4)
International Journal of Hematology Research     Open Access   (Followers: 2)
International Journal of Hematology-Oncology and Stem Cell Research     Open Access   (Followers: 2)
International Journal of Laboratory Hematology     Hybrid Journal   (Followers: 25)
Iraqi Journal of Hematology     Open Access  
JMIR Diabetes     Open Access  
Journal of Blood Disorders & Transfusion     Open Access   (Followers: 3)
Journal of Applied Hematology     Open Access   (Followers: 2)
Journal of Blood Medicine     Open Access   (Followers: 1)
Journal of Cerebral Blood Flow & Metabolism     Hybrid Journal   (Followers: 3)
Journal of Diabetes     Open Access   (Followers: 20)
Journal of Diabetes and its Complications     Hybrid Journal   (Followers: 25)
Journal of Diabetes and Metabolic Disorders     Open Access   (Followers: 8)
Journal of Diabetes Investigation     Open Access   (Followers: 12)
Journal of Diabetes Mellitus     Open Access   (Followers: 5)
Journal of Diabetes Research     Open Access   (Followers: 13)
Journal of Diabetes Research     Open Access   (Followers: 9)
Journal of Hematological Malignancies     Open Access  
Journal of Hematology     Open Access   (Followers: 2)
Journal of Hematology and Transfusion Medicine     Open Access   (Followers: 1)
Journal of Hematopathology     Hybrid Journal   (Followers: 3)
Journal of Hypo & Hyperglycemia     Partially Free  
Journal of Pediatric Hematology/Oncology     Hybrid Journal   (Followers: 8)
Journal of Social Health and Diabetes     Open Access   (Followers: 1)
Journal of Thrombosis and Haemostasis     Hybrid Journal   (Followers: 81)
Journal of Thrombosis and Thrombolysis     Hybrid Journal   (Followers: 35)
Journal of Transfusion Medicine     Full-text available via subscription  
Kidney and Blood Pressure Research     Open Access   (Followers: 4)
Leukemia     Hybrid Journal   (Followers: 22)
Leukemia and Lymphoma     Hybrid Journal   (Followers: 12)
Leukemia Research     Hybrid Journal   (Followers: 8)
Leukemia Research Reports     Open Access   (Followers: 1)
Leukemia Supplements     Full-text available via subscription  
Mediterranean Journal of Hematology and Infectious Diseases     Open Access  
Nederlands Tijdschrift voor Diabetologie     Hybrid Journal  
Nutrition & Diabetes     Open Access   (Followers: 20)
Oncohematology     Open Access   (Followers: 1)
Open Diabetes Journal     Open Access  
Open Hematology Journal     Open Access   (Followers: 1)
Open Hypertension Journal     Open Access  
Open Journal of Blood Diseases     Open Access  
Pediatric Blood & Cancer     Hybrid Journal   (Followers: 8)
Pediatric Hematology Oncology Journal     Open Access   (Followers: 3)
Peritoneal Dialysis International     Hybrid Journal  
Platelets     Hybrid Journal   (Followers: 3)
Practical Diabetes     Hybrid Journal   (Followers: 7)
Primary Care Diabetes     Hybrid Journal   (Followers: 26)
Research & Reviews : Journal of Oncology and Hematology     Full-text available via subscription   (Followers: 1)
Research and Practice in Thrombosis and Haemostasis     Open Access   (Followers: 1)
Revista Cubana de Hematología, Inmunología y Hemoterapia     Open Access  
Seminars in Hematology     Hybrid Journal   (Followers: 12)
Seminars in Thrombosis and Hemostasis     Hybrid Journal   (Followers: 45)
Thalassemia Reports     Open Access   (Followers: 1)
The Lancet Haematology     Full-text available via subscription   (Followers: 38)
Therapeutic Advances in Hematology     Hybrid Journal  
Thrombosis & Haemostasis     Hybrid Journal   (Followers: 145)
Thrombosis Research     Hybrid Journal   (Followers: 47)
Transfusionsmedizin - Immunhämatologie, Hämotherapie, Immungenetik, Zelltherapie     Hybrid Journal  
Transplantation and Cellular Therapy     Hybrid Journal   (Followers: 13)
Veins and Lymphatics     Open Access   (Followers: 1)

           

Similar Journals
Journal Cover
Arteriosclerosis, Thrombosis and Vascular Biology
Journal Prestige (SJR): 3.435
Citation Impact (citeScore): 5
Number of Followers: 29  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 1079-5642 - ISSN (Online) 1524-4636
Published by American Heart Association Homepage  [12 journals]
  • Regulated Necrosis in Atherosclerosis

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      Authors: Pauline Puylaert Michelle Zurek Katey J. Rayner Guido R.Y. De Meyer Wim Martinet Laboratory of Physiopharmacology; Inflammation, Faculty of Medicine, University of Ottawa, ON, Canada (K.J.R.). University of Ottawa Heart Institute, ON, Canada (K.J.R.).
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.
      During atherosclerosis, lipid-rich plaques are formed in large- and medium-sized arteries, which can reduce blood flow to tissues. This situation becomes particularly precarious when a plaque develops an unstable phenotype and becomes prone to rupture. Despite advances in identifying and treating vulnerable plaques, the mortality rate and disability caused by such lesions remains the number one health threat in developed countries. Vulnerable, unstable plaques are characterized by a large necrotic core, implying a prominent role for necrotic cell death in atherosclerosis and plaque destabilization. Necrosis can occur accidentally or can be induced by tightly regulated pathways. Over the past decades, different forms of regulated necrosis, including necroptosis, ferroptosis, pyroptosis, and secondary necrosis, have been identified, and these may play an important role during atherogenesis. In this review, we describe several forms of necrosis that may occur in atherosclerosis and how pharmacological modulation of these pathways can stabilize vulnerable plaques. Moreover, some challenges of targeting necrosis in atherosclerosis such as the presence of multiple death-inducing stimuli in plaques and extensive cross-talk between necrosis pathways are discussed. A better understanding of the role of (regulated) necrosis in atherosclerosis and the mechanisms contributing to plaque destabilization may open doors to novel pharmacological strategies and will enable clinicians to tackle the residual cardiovascular risk that remains in many atherosclerosis patients.
      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-09-22T09:00:05Z
      DOI: 10.1161/ATVBAHA.122.318177
       
  • Lipoproteins and Calcific Aortic Valve Disease: Hardening Evidence'

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      Authors: Kevin D. O’Brien Division of Cardiology; Department of Medicine; UW Medicine Heart Institute UW Medicine Diabetes Institute, University of Washington, Seattle.
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.

      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-09-22T09:00:05Z
      DOI: 10.1161/ATVBAHA.122.318310
       
  • Aspirin for the Primary Prevention of Cardiovascular Disease: Time for a
           Platelet-Guided Approach

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      Authors: Lucas B. Cofer Tessa J. Barrett Jeffrey S. Berger NYU Grossman School of Medicine.
      First page: 1207
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.
      Aspirin protects against atherothrombosis while increasing the risk of major bleeding. Although it is widely used to prevent cardiovascular disease (CVD), its benefit does not outweigh its risk for primary CVD prevention in large population settings. The recent United States Preventive Services Task Force guidelines on aspirin use to prevent CVD reflect this clinical tradeoff as well as the persistent struggle to define a population that would benefit from prophylactic aspirin therapy. Past clinical trials of primary CVD prevention with aspirin have not included consideration of a biomarker relevant to aspirin’s mechanism of action, platelet inhibition. This approach is at odds with the paradigm used in other key areas of pharmacological CVD prevention, including antihypertensive and statin therapy, which combine cardiovascular risk assessment with the measurement of mechanistic biomarkers (eg, blood pressure and LDL [low-density lipoprotein]-cholesterol). Reliable methods for quantifying platelet activity, including light transmission aggregometry and platelet transcriptomics, exist and should be considered to identify individuals at elevated cardiovascular risk due to a hyperreactive platelet phenotype. Therefore, we propose a new, platelet-guided approach to the study of prophylactic aspirin therapy. We think that this new approach will reveal a population with hyperreactive platelets who will benefit most from primary CVD prevention with aspirin and usher in a new era of precision-guided antiplatelet therapy.
      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-09-01T09:00:03Z
      DOI: 10.1161/ATVBAHA.122.318020
       
  • An Aspirin a Day…

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      Authors: James D. McFadyen Elizabeth E. Gardiner Atherothrombosis; Cancer, the John Curtin School of Medical Research, The Australian National University, Canberra (E.E.G.).
      First page: 1217
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.

      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-09-01T09:00:03Z
      DOI: 10.1161/ATVBAHA.122.318337
       
  • Ceramide Metabolism in Cardiovascular Disease: A Network With High
           Therapeutic Potential

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      Authors: Andreas Zietzer Philip Düsing Laurine Reese Georg Nickenig Felix Jansen Department of Internal Medicine II; University Hospital Bonn, University of Bonn, Germany.
      First page: 1220
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.
      Growing evidence suggests that ceramides play an important role in the development of atherosclerotic and valvular heart disease. Ceramides are biologically active sphingolipids that are produced by a complex network of enzymes. Lowering cellular and tissue levels of ceramide by inhibiting the ceramide-producing enzymes counteracts atherosclerotic and valvular heart disease development in animal models. In vascular tissues, ceramides are produced in response to hyperglycemia and TNF (tumor necrosis factor)-α signaling and are involved in NO-signaling and inflammation. In humans, elevated blood ceramide levels are associated with cardiovascular events. Furthermore, important cardiovascular risk factors, such as obesity and diabetes, have been linked to ceramide accumulation. This review summarizes the basic mechanisms of how ceramides drive cardiovascular disease locally and links these findings to the intriguing results of human studies on ceramides as biomarkers for cardiovascular events. Moreover, we discuss the current state of interventions to therapeutically influence vascular ceramide metabolism, both locally and systemically.
      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-08-25T09:00:02Z
      DOI: 10.1161/ATVBAHA.122.318048
       
  • PLC (Phospholipase C) β2 Promotes VEGF (Vascular Endothelial Growth
           Factor)–Induced Vascular Permeability

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      Authors: Kathryn N. Phoenix Zhichao Yue Lixia Yue Chunxia G. Cronin Bruce T. Liang Luke H. Hoeppner Kevin P. Claffey Center for Vascular Biology; Department of Cell Biology, University of Connecticut Health Center, Farmington. (K.N.P., K.P.C.) Pat Jim Calhoun Cardiology Center, University of Connecticut Health Center, Farmington. (Z.Y., L.Y., C.G.C., B.T.L.) The Hormel Institute, University of Minnesota, Austin (L.H.H.). Masonic Cancer Center, University of Minnesota, Minneapolis (L.H.H.).
      First page: 1229
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.
      Background:Regulation of vascular permeability is critical to maintaining tissue metabolic homeostasis. VEGF (vascular endothelial growth factor) is a key stimulus of vascular permeability in acute and chronic diseases including ischemia reperfusion injury, sepsis, and cancer. Identification of novel regulators of vascular permeability would allow for the development of effective targeted therapeutics for patients with unmet medical need.Methods:In vitro and in vivo models of VEGFA-induced vascular permeability, pathological permeability, quantitation of intracellular calcium release and cell entry, and phosphatidylinositol 4,5-bisphosphate levels were evaluated with and without modulation of PLC (phospholipase C) β2.Results:Global knock-out of PLCβ2 in mice resulted in blockade of VEGFA-induced vascular permeability in vivo and transendothelial permeability in primary lung endothelial cells. Further work in an immortalized human microvascular cell line modulated with stable knockdown of PLCβ2 recapitulated the observations in the mouse model and primary cell assays. Additionally, loss of PLCβ2 limited both intracellular release and extracellular entry of calcium following VEGF stimulation as well as reduced basal and VEGFA-stimulated levels of phosphatidylinositol 4,5-bisphosphate compared to control cells. Finally, loss of PLCβ2 in both a hyperoxia-induced lung permeability model and a cardiac ischemia:reperfusion model resulted in improved animal outcomes when compared with wild-type controls.Conclusions:The results implicate PLCβ2 as a key positive regulator of VEGF-induced vascular permeability through regulation of both calcium flux and phosphatidylinositol 4,5-bisphosphate levels at the cellular level. Targeting of PLCβ2 in a therapeutic setting may provide a novel approach to regulating vascular permeability in patients.
      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-07-21T09:00:06Z
      DOI: 10.1161/ATVBAHA.122.317645
       
  • Novel Target for Limiting VEGF-A (Vascular Endothelial Growth Factor
           A)–Induced Vascular Permeability

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      Authors: Joyce Bischoff Vascular Biology Program; Department of Surgery, Boston Children’s Hospital, Boston, MA (J.B.). Department of Surgery, Harvard Medical School, Boston, MA (J.B.).
      First page: 1242
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.

      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-08-25T09:00:02Z
      DOI: 10.1161/ATVBAHA.122.318105
       
  • Nonproteolytic Intracellular Domain of MT1-MMP (Membrane-Type 1 Matrix
           Metalloproteinase) Coordinately Modulates Abdominal Aortic Aneurysm and
           Atherosclerosis to Mice

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      Authors: Michele Silvestro Cristobal F. Rivera Dornazsadat Alebrahim John Vlahos Muhammad Yogi Pratama Cuijie Lu Claudia Tang Zander Harpel Rayan Sleiman Tellaoui Ariadne L. Zias Delphina J. Maldonado Devon Byrd Mukundan Attur Paolo Mignatti Bhama Ramkhelawon Division of Vascular; Endovascular Surgery, Department of Surgery, New York University Langone Medical Center, New York. (M.S., C.F.R., D.A., J.V., M.Y.P., C.T., Z.H., R.S.T., A.L.Z., D.J.M., D.B., B.R.) Division of Rheumatology, Department of Medicine, New York University Langone Medical Center, New York. (C.L., M.A., P.M.) Department of Cell Biology, New York University Langone Medical Center, New York. (P.M., B.R.)
      First page: 1244
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.
      Background:MT1-MMP (membrane-type 1 matrix metalloproteinase, MMP-14) is a transmembrane-anchored protein with an extracellular proteinase domain and a cytoplasmic tail devoid of proteolytic functions but capable of mediating intracellular signaling that regulates tissue homeostasis. MT1-MMP extracellular proteolytic activity has been shown to regulate pathological remodeling in aortic aneurysm and atherosclerosis. However, the role of the nonproteolytic intracellular domain of MT1-MMP in vascular remodeling in abdominal aortic aneurysms (AAA) is unknown.Methods:We generated a mutant mouse that harbors a point mutation (Y573D) in the MT1-MMP cytoplasmic domain that abrogates the MT1-MMP signaling function without affecting its proteolytic activity. These mice and their control wild-type littermates were subjected to experimental AAA modeled by angiotensin II infusion combined with PCSK9 (proprotein convertase subtilisin/kexin type 9) overexpression and high-cholesterol feeding.Results:The mutant mice developed more severe AAA than the control mice, with concomitant generation of intraaneurysmal atherosclerotic lesions and dramatically increased macrophage infiltration and elastin degradation. Aortic lesion-associated and bone marrow–derived macrophages from the mutant mice exhibited an enhanced inflammatory state and expressed elevated levels of proinflammatory Netrin-1, a protein previously demonstrated to promote both atherosclerosis and AAA.Conclusions:Our findings show that the cytoplasmic domain of MT1-MMP safeguards from AAA and atherosclerotic plaque development through a proteolysis-independent signaling mechanism associated with Netrin-1 expression. This unexpected function of MT1-MMP unveils a novel mechanism of synchronous onset of AAA and atherogenesis and highlights its importance in the control of vascular wall homeostasis.
      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-09-08T09:00:05Z
      DOI: 10.1161/ATVBAHA.122.317686
       
  • Inhibition of the Renin-Angiotensin System Fails to Suppress
           β-Aminopropionitrile–Induced Thoracic Aortopathy in Mice

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      Authors: Hisashi Sawada Satoko Ohno-Urabe Dien Ye Michael K. Franklin Jessica J. Moorleghen Deborah A. Howatt Adam E. Mullick Alan Daugherty Hong S. Lu Saha Cardiovascular Research Center (H.S; S.O.-U, M.K.F, J.J.M, D.A.H, A.D, H.S.L.) Saha Aortic Center (H.S, M.K.F, J.J.M, D.A.H, A.D, H.S.L.) Department of Physiology, University of Kentucky, Lexington (H.S, A.D, H.S.L.). Ionis Pharmaceuticals, Carlsbad, CA (A.E.M.).
      First page: 1254
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.
      BACKGROUND:Cross-linking of lysine residues in elastic and collagen fibers is a vital process in aortic development. Inhibition of lysyl oxidase by β-aminopropionitrile leads to thoracic aortopathies in mice. Although the renin-angiotensin system contributes to several types of thoracic aortopathies, it remains unclear whether inhibition of the renin-angiotensin system protects against aortopathy caused by the impairment of elastic fiber/collagen crosslinking.METHODS:β-aminopropionitrile (0.5% wt/vol) was started in drinking water to induce aortopathies in male C57BL/6J mice at 4 weeks of age for 4 weeks. Five approaches were tested to investigate the impact of the renin-angiotensin system. Bulk RNA sequencing was performed to explore potential molecular mechanisms of β-aminopropionitrile–induced thoracic aortopathies.RESULTS:Losartan increased plasma renin concentrations significantly, compared with vehicle-infused mice, indicating effective angiotensin II type 1 receptor inhibition. However, losartan did not suppress β-aminopropionitrile–induced aortic rupture and dilatation. Since losartan is a surmountable inhibitor, irbesartan, an insurmountable inhibitor, was also tested. Although increased plasma renin concentrations indicated effective inhibition, irbesartan did not ameliorate aortic rupture and dilatation in β-aminopropionitrile-administered mice. Thus, β-aminopropionitrile–induced thoracic aortopathies were refractory to angiotensin II type 1 receptor inhibition. Next, we inhibited angiotensin II production by pharmacological or genetic depletion of angiotensinogen, the unique precursor of angiotensin II. However, neither suppressed β-aminopropionitrile–induced thoracic aortic rupture and dilatation. Aortic RNA sequencing revealed molecular changes during β-aminopropionitrile administration that were distinct from other types of aortopathies in which angiotensin II type 1 receptor inhibition protects against aneurysm formation.CONCLUSIONS:Inhibition of either angiotensin II action or production of the renin-angiotensin system does not attenuate β-aminopropionitrile–induced thoracic aortopathies in mice.
      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-08-25T09:00:02Z
      DOI: 10.1161/ATVBAHA.122.317712
       
  • Variants in the GPR146 Gene Are Associated With a Favorable
           Cardiometabolic Risk Profile

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      Authors: Antoine Rimbert Ming W. Yeung Nawar Dalila Chris H.L. Thio Haojie Yu Natalia Loaiza Federico Oldoni Adriaan van der Graaf Siqi Wang M. Abdullah Said Lisanne L. Blauw Aurore Girardeau Lise Bray Amandine Caillaud Vincent W. Bloks Marie Marrec Philippe Mouli Patrick C.N. Rensen Bart van de Sluis Harold Snieder Mathilde Di Filippo Pim van der Harst Anne Tybjaerg-Hansen Philippe Zimmerman Bertrand Cariou Jan Kuivenhoven Nantes Université; CHU Nantes, CNRS, INSERM, l’institut du thorax, France (A.R., A.G., L.B., A.C., M.M., B.C.). Department of Cardiology, University Medical Center Groningen, University of Groningen, the Netherlands. (M.W.Y., S.W., M.S., P.v.d.H.) Department of Pediatrics, Section Molecular Genetics, University Medical Center Groningen, University of Groningen, the Netherlands. (N.L., B.v.d.S., J.K.) Department of Genetics, University Medical Center Groningen, University of Groningen, the Netherlands. (A.v.d.G.) Department of Epidemiology, University Medical Center Groningen, University of Groningen, the Netherlands. (C.H.L.T., S.W., H.S.) Sections of Molecular Metabolism Frederiksberg Hospital, Denmark (A.T.-H.). NEBION AG, Zurich, Switzerland (P.Z.).
      First page: 1262
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.
      BACKGROUND:In mice, GPR146 (G-protein–coupled receptor 146) deficiency reduces plasma lipids and protects against atherosclerosis. Whether these findings translate to humans is unknown.METHODS:Common and rare genetic variants in theGPR146gene locus were used as research instruments in the UK-Biobank. The Lifelines, and The Copenhagen-City Heart Study, and a cohort of individuals with familial hypobetalipoproteinemia were used to find and study rareGPR146variants.RESULTS:In the UK-Biobank, carriers of the common rs2362529-C allele present with lower low-density lipoprotein cholesterol, apo (apolipoprotein) B, high-density lipoprotein cholesterol, apoAI, CRP (C-reactive protein), and plasma liver enzymes compared with noncarriers. Carriers of the common rs1997243-G allele, associated with higher GPR146 expression, present with the exact opposite phenotype. The associations with plasma lipids of the above alleles are allele dose-dependent. Heterozygote carriers of a rare coding variant (p.Pro62Leu; n=2615), predicted to be damaging, show a stronger reductions in the above parameters compared with carriers of the common rs2362529-C allele. The p.Pro62Leu variant is furthermore shown to segregate with low low-density lipoprotein cholesterol in a family with familial hypobetalipoproteinemia. Compared with controls, carriers of the common rs2362529-C allele show a marginally reduced risk of coronary artery disease (P=0.03) concomitant with a small effect size on low-density lipoprotein cholesterol (average decrease of 2.24 mg/dL in homozygotes) of this variant. Finally, mendelian randomization analyses suggest a causal relationship betweenGPR146gene expression and plasma lipid and liver enzyme levels.CONCLUSIONS:This study shows that carriers of new geneticGPR146variants have a beneficial cardiometabolic risk profile, but it remains to be shown whether genetic or pharmaceutical inhibition of GPR146 protects against atherosclerosis in humans.
      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-09-01T09:00:03Z
      DOI: 10.1161/ATVBAHA.122.317514
       
  • High-Density Lipoprotein and Long-Term Incidence and Progression of Aortic
           Valve Calcification: The Multi-Ethnic Study of Atherosclerosis

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      Authors: Anna E. Bortnick Petra Buzkova James Otvos Majken Jensen Michael Y. Tsai Matthew Budoff Rachel Mackey Samar R. El Khoudary Elda Favari Ryung S. Kim Carlos J. Rodriguez George Thanassoulis Jorge R. Kizer Department of Medicine; Division of Cardiology, Albert Einstein College of Medicine, Bronx NY. (A.E.B., C.J.R.) Division of Geriatrics, Albert Einstein College of Medicine, Bronx NY. (A.E.B.) Department of Epidemiology Biostatistics, University of California‚ San Francisco (J.R.K.).
      First page: 1272
      Abstract: Arteriosclerosis, Thrombosis, and Vascular Biology, Ahead of Print.
      Background:Aortic valve calcification (AVC) shares pathological features with atherosclerosis. Lipoprotein components have been detected in aortic valve tissue, including HDL (high-density lipoprotein). HDL measures have inverse associations with cardiovascular disease, but relationships with long-term AVC progression are unclear. We investigated associations of HDL cholesterol, particles, apoC3-defined HDL subtypes, and, secondarily, CETP (cholesteryl ester transfer protein) mass and activity, with long-term incidence and progression of AVC.Methods:We used linear mixed-effects models to evaluate the associations of baseline HDL indices with AVC. AVC was quantified by Agatston scoring of up to 3 serial computed tomography scans over a median of 8.9 (maximum 11.2) years of follow-up in the Multi-Ethnic Study of Atherosclerosis (n=6814).Results:After adjustment, higher concentrations of HDL-C (high-density lipoprotein cholesterol), HDL-P (HDL particles), large HDL-P, and apoC3-lacking HDL-C were significantly associated with lower incidence/progression of AVC, as was higher CETP mass. Neither small nor medium HDL-P, apoC3-containing HDL-C, or CETP activity were significantly associated with AVC incidence/progression in the main analyses. When included together, a significant association was observed only for HDL-C, but not for HDL-P. In exploratory analyses, inverse associations for HDL-C, HDL-P, large HDL-P, and apocC3-lacking HDL with AVC incidence/progression were more pronounced for adults ≥65 years, men, and White participants. ApoC3-containing HDL-C only showed a positive association with AVC in these subgroups.Conclusions:In a multiethnic population, HDL-C, HDL-P, large HDL-P, and apoC3-lacking HDL-C were inversely associated with long-term incidence and progression of AVC. Further investigation of HDL composition and mechanisms could be useful in understanding pathways that slow AVC.
      Citation: Arteriosclerosis, Thrombosis, and Vascular Biology
      PubDate: 2022-08-18T09:00:02Z
      DOI: 10.1161/ATVBAHA.122.318004
       
 
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