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Endothelial dysfunction and panvascular diseases

  • 1.

    Department of Endocrinology,The First Affiliated Hospital of USTC(Anhui Provincial Hospital), Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China

  • 2.

    Department of Cardiology, The First Affiliated Hospital of USTC(Anhui Provincial Hospital), Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China

  • 3.

    Department of Cardiology,Institute of Panvascular Medicine, Zhong Shan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai 200032, China

Cite this:
https://doi.org/10.52396/JUST-2021-0051
  • Publish Date: 31 August 2021
    Abstract

  • Abstract

    Vascular endothelial cells are the key cell type responsible for vascular health and homeostasis. Endothelial dysfunction (ED), as the core process of panvascular diseases, is caused by multi-step and multi-risk factors involving endothelial injury, hyperpermeability, vasoconstriction, inflammation, oxidative stress, leukocyte adhesion, metabolic disorder, endothelial-to-mesenchymal transition (EndMT), and platelet activation. ED plays an important role in cardiovascular, tumor, metabolic, pulmonary, and infectious diseases. Therefore, the assessment of endothelial function is of great importance to clinical diagnosis and therapeutics. In this review, we centered on the relationship between ED and panvascular diseases, and overviewed the research advance of ED and panvascular diseases, with an aim to understanding the novel molecular mechanism of panvascular diseases and accelerating the development of pharmaceuticals targeting ED in panvascular diseases.

    Abstract

    Vascular endothelial cells are the key cell type responsible for vascular health and homeostasis. Endothelial dysfunction (ED), as the core process of panvascular diseases, is caused by multi-step and multi-risk factors involving endothelial injury, hyperpermeability, vasoconstriction, inflammation, oxidative stress, leukocyte adhesion, metabolic disorder, endothelial-to-mesenchymal transition (EndMT), and platelet activation. ED plays an important role in cardiovascular, tumor, metabolic, pulmonary, and infectious diseases. Therefore, the assessment of endothelial function is of great importance to clinical diagnosis and therapeutics. In this review, we centered on the relationship between ED and panvascular diseases, and overviewed the research advance of ED and panvascular diseases, with an aim to understanding the novel molecular mechanism of panvascular diseases and accelerating the development of pharmaceuticals targeting ED in panvascular diseases.
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    • References(30)
  • [1]
    葛均波, 王拥军. 泛血管医学——概念及常见疾病诊治. 北京: 人民卫生出版社, 2018.
    [2]
    Inagami T, Naruse M, Hoover R. Endothelium as an endocrine organ.Annu. Rev. Physiol., 1995, 57: 171-189.
    [3]
    Rajendran P, Rengarajan T, Thangavel J, et al. The vascular endothelium and human diseases. Int. J. Biol. Sci., 2013, 9(10): 1057-1069.
    [4]
    Xu S, Ilyas I, Little P J, et al. Endothelial dysfunction in atherosclerotic cardiovascular diseases and beyond: From mechanism to pharmacotherapies. Pharmacol. Rev., 2021, 73(3):924-967.
    [5]
    Bidault G, Garcia M, Capeau J, et al. Progerin expression induces inflammation, oxidative stress and senescence in human coronary endothelial cells. Cells, 2020, 9(5): 1201.
    [6]
    Kotla S, Le N T, Vu H T, et al. Endothelial senescence-associated secretory phenotype (SASP) is regulated by Makorin-1 ubiquitin E3 ligase. Metabolism, 2019, 100: 153962.
    [7]
    Luo X, Bai Y, He S, et al. Sirtuin 1 ameliorates defenestration in hepatic sinusoidal endothelial cells during liver fibrosis via inhibiting stress-induced premature senescence. Cell Prolif., 2021, 54(3): e12991.
    [8]
    Lanzer P, Topol E J. Panvascular Medicine: Integrated Clinical Management. Berlin: Springer-Verlag, 2002.
    [9]
    杨靖,王克强,霍勇, 等,《泛血管疾病综合防治科学声明》工作组. 泛血管疾病综合防治科学声明. 中国循环杂志, 2019, 34: 1041-1046.
    Yang Jing, Wang Keqiang, Huo Yong, et al, on behalf of the working group on scientific statement for the prevention and treatment of panvascular disease. Scientific statement for the prevention and treatment of panvascular disease. Chinese Circulation Journal, 2019, 34: 1041-1046.
    [10]
    韩雅玲.以科技创新驱动引领我国心血管病领域高质量发展. 中华心血管病杂志, 2021, 49: 1-2.
    [11]
    中国心血管健康与疾病报告编写组. 中国心血管健康与疾病报告2019概要. 中国循环杂志, 2020, 35: 833-854.
    The Writing Committee of the Report on Cardiovascular Health and Diseases in China. Report on cardiovascular health and diseases in China 2019:an updated summary. Chinese Circulation Journal, 2020, 35: 833-854.
    [12]
    Akhmedov A, Sawamura T, Chen C H, et al. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1): a crucial driver of atherosclerotic cardiovascular disease. Eur. Heart J., 2021; doi: 10.1093/eurheartj/ehaa770.
    [13]
    Brunt V E, Gioscia-Ryan R A, Casso A G, et al. Trimethylamine-N-oxide promotes age-related vascular oxidative stress and endothelial dysfunction in mice and healthy humans. Hypertension, 2020, 76(1): 101-112.
    [14]
    Chen M L, Zhu X H, Ran L, et al. Trimethylamine-N-oxide induces vascular inflammation by activating the NLRP3 inflammasome through the SIRT3-SOD2-mtROS signaling pathway. J. Am. Heart Assoc., 2017, 6(9): e006347.
    [15]
    Cheng X, Qiu X, Liu Y, et al. Trimethylamine N-oxide promotes tissue factor expression and activity in vascular endothelial cells: A new link between trimethylamine N-oxide and atherosclerotic thrombosis. Thromb. Res., 2019, 177: 110-116.
    [16]
    Vergallo R, Crea F. Atherosclerotic plaque healing. N. Engl. J. Med., 2020, 383: 846-857.
    [17]
    Vergallo R, Crea F. Atherosclerotic plaque disruption and healing. Eur. Heart J., 2020, 41(42): 4079-4080.
    [18]
    刘臻臻, 罗琪. 肿瘤血管靶向治疗策略的新进展. 世界华人消化杂志, 2010, 18: 2889-2893.
    Liu Zhenzhen, Luo Qi. Recent advances in research of vascular targeting strategy for tumor therapy. World Chinese Journal of Digestology, 2010, 18: 2889-2893.
    [19]
    Zhang S, Kim J Y, Xu S, et al. Endothelial-specific YY1 governs sprouting angiogenesis through directly interacting with RBPJ. Proc. Natl. Acad. Sci. U. S. A., 2020, 117(9): 4792-4801.
    [20]
    Liu H, Qiu Y, Pei X, et al. Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth. Sci. Rep., 2020, 10(1): 20493.
    [21]
    Liu Z, Ma X, Ilyas I, et al. Impact of sodium glucose cotransporter 2 (SGLT2) inhibitors on atherosclerosis: from pharmacology to pre-clinical and clinical therapeutics. Theranostics, 2021, 11(9): 4502-4515.
    [22]
    翁建平.代谢性肝病的定义与分类探讨. 中华医学杂志, 2020, 100: 401-405.
    Weng Jianping. The definition and classification of metabolic liver disease. National Medical Journal of China, 2020, 100: 401-405.
    [23]
    Hammoutene A, Rautou P E. Role of liver sinusoidal endothelial cells in non-alcoholic fatty liver disease. J. Hepatol., 2019, 70(6): 1278-1291.
    [24]
    Libby P, Lüscher T. COVID-19 is, in the end, an endothelial disease. Eur. Heart J., 2020, 41(32): 3038-3044.
    [25]
    Chung M K, Zidar D A, Bristow M R, et al. COVID-19 and cardiovascular disease: From bench to bedside. Circ. Res., 2021, 128(8): 1214-1236.
    [26]
    Varga Z, Flammer A J, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet, 2020, 395(10234): 1417-1418.
    [27]
    Zhang J, He Y, Yan X, et al. MicroRNA-483 amelioration of experimental pulmonary hypertension. EMBO Mol. Med., 2020, 12(5): e11303.
    [28]
    Jia C, Zhang J, Chen H, et al. Endothelial cell pyroptosis plays an important role in Kawasaki disease via HMGB1/RAGE/cathespin B signaling pathway and NLRP3 inflammasome activation. Cell Death Dis., 2019, 10(10): 778.
    [29]
    Cao X, Xue L D, Di Y, et al. MSC-derived exosomal lncRNA SNHG7 suppresses endothelial-mesenchymal transition and tube formation in diabetic retinopathy via miR-34a-5p/XBP1 axis. Life Sci., 2021, 272: 119232.
    [30]
    McCann J V, Liu A, Musante L, et al. A miRNA signature in endothelial cell-derived extracellular vesicles in tumor-bearing mice. Sci. Rep., 2019, 9(1): 16743.
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    [1]
    葛均波, 王拥军. 泛血管医学——概念及常见疾病诊治. 北京: 人民卫生出版社, 2018.
    [2]
    Inagami T, Naruse M, Hoover R. Endothelium as an endocrine organ.Annu. Rev. Physiol., 1995, 57: 171-189.
    [3]
    Rajendran P, Rengarajan T, Thangavel J, et al. The vascular endothelium and human diseases. Int. J. Biol. Sci., 2013, 9(10): 1057-1069.
    [4]
    Xu S, Ilyas I, Little P J, et al. Endothelial dysfunction in atherosclerotic cardiovascular diseases and beyond: From mechanism to pharmacotherapies. Pharmacol. Rev., 2021, 73(3):924-967.
    [5]
    Bidault G, Garcia M, Capeau J, et al. Progerin expression induces inflammation, oxidative stress and senescence in human coronary endothelial cells. Cells, 2020, 9(5): 1201.
    [6]
    Kotla S, Le N T, Vu H T, et al. Endothelial senescence-associated secretory phenotype (SASP) is regulated by Makorin-1 ubiquitin E3 ligase. Metabolism, 2019, 100: 153962.
    [7]
    Luo X, Bai Y, He S, et al. Sirtuin 1 ameliorates defenestration in hepatic sinusoidal endothelial cells during liver fibrosis via inhibiting stress-induced premature senescence. Cell Prolif., 2021, 54(3): e12991.
    [8]
    Lanzer P, Topol E J. Panvascular Medicine: Integrated Clinical Management. Berlin: Springer-Verlag, 2002.
    [9]
    杨靖,王克强,霍勇, 等,《泛血管疾病综合防治科学声明》工作组. 泛血管疾病综合防治科学声明. 中国循环杂志, 2019, 34: 1041-1046.
    Yang Jing, Wang Keqiang, Huo Yong, et al, on behalf of the working group on scientific statement for the prevention and treatment of panvascular disease. Scientific statement for the prevention and treatment of panvascular disease. Chinese Circulation Journal, 2019, 34: 1041-1046.
    [10]
    韩雅玲.以科技创新驱动引领我国心血管病领域高质量发展. 中华心血管病杂志, 2021, 49: 1-2.
    [11]
    中国心血管健康与疾病报告编写组. 中国心血管健康与疾病报告2019概要. 中国循环杂志, 2020, 35: 833-854.
    The Writing Committee of the Report on Cardiovascular Health and Diseases in China. Report on cardiovascular health and diseases in China 2019:an updated summary. Chinese Circulation Journal, 2020, 35: 833-854.
    [12]
    Akhmedov A, Sawamura T, Chen C H, et al. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1): a crucial driver of atherosclerotic cardiovascular disease. Eur. Heart J., 2021; doi: 10.1093/eurheartj/ehaa770.
    [13]
    Brunt V E, Gioscia-Ryan R A, Casso A G, et al. Trimethylamine-N-oxide promotes age-related vascular oxidative stress and endothelial dysfunction in mice and healthy humans. Hypertension, 2020, 76(1): 101-112.
    [14]
    Chen M L, Zhu X H, Ran L, et al. Trimethylamine-N-oxide induces vascular inflammation by activating the NLRP3 inflammasome through the SIRT3-SOD2-mtROS signaling pathway. J. Am. Heart Assoc., 2017, 6(9): e006347.
    [15]
    Cheng X, Qiu X, Liu Y, et al. Trimethylamine N-oxide promotes tissue factor expression and activity in vascular endothelial cells: A new link between trimethylamine N-oxide and atherosclerotic thrombosis. Thromb. Res., 2019, 177: 110-116.
    [16]
    Vergallo R, Crea F. Atherosclerotic plaque healing. N. Engl. J. Med., 2020, 383: 846-857.
    [17]
    Vergallo R, Crea F. Atherosclerotic plaque disruption and healing. Eur. Heart J., 2020, 41(42): 4079-4080.
    [18]
    刘臻臻, 罗琪. 肿瘤血管靶向治疗策略的新进展. 世界华人消化杂志, 2010, 18: 2889-2893.
    Liu Zhenzhen, Luo Qi. Recent advances in research of vascular targeting strategy for tumor therapy. World Chinese Journal of Digestology, 2010, 18: 2889-2893.
    [19]
    Zhang S, Kim J Y, Xu S, et al. Endothelial-specific YY1 governs sprouting angiogenesis through directly interacting with RBPJ. Proc. Natl. Acad. Sci. U. S. A., 2020, 117(9): 4792-4801.
    [20]
    Liu H, Qiu Y, Pei X, et al. Endothelial specific YY1 deletion restricts tumor angiogenesis and tumor growth. Sci. Rep., 2020, 10(1): 20493.
    [21]
    Liu Z, Ma X, Ilyas I, et al. Impact of sodium glucose cotransporter 2 (SGLT2) inhibitors on atherosclerosis: from pharmacology to pre-clinical and clinical therapeutics. Theranostics, 2021, 11(9): 4502-4515.
    [22]
    翁建平.代谢性肝病的定义与分类探讨. 中华医学杂志, 2020, 100: 401-405.
    Weng Jianping. The definition and classification of metabolic liver disease. National Medical Journal of China, 2020, 100: 401-405.
    [23]
    Hammoutene A, Rautou P E. Role of liver sinusoidal endothelial cells in non-alcoholic fatty liver disease. J. Hepatol., 2019, 70(6): 1278-1291.
    [24]
    Libby P, Lüscher T. COVID-19 is, in the end, an endothelial disease. Eur. Heart J., 2020, 41(32): 3038-3044.
    [25]
    Chung M K, Zidar D A, Bristow M R, et al. COVID-19 and cardiovascular disease: From bench to bedside. Circ. Res., 2021, 128(8): 1214-1236.
    [26]
    Varga Z, Flammer A J, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet, 2020, 395(10234): 1417-1418.
    [27]
    Zhang J, He Y, Yan X, et al. MicroRNA-483 amelioration of experimental pulmonary hypertension. EMBO Mol. Med., 2020, 12(5): e11303.
    [28]
    Jia C, Zhang J, Chen H, et al. Endothelial cell pyroptosis plays an important role in Kawasaki disease via HMGB1/RAGE/cathespin B signaling pathway and NLRP3 inflammasome activation. Cell Death Dis., 2019, 10(10): 778.
    [29]
    Cao X, Xue L D, Di Y, et al. MSC-derived exosomal lncRNA SNHG7 suppresses endothelial-mesenchymal transition and tube formation in diabetic retinopathy via miR-34a-5p/XBP1 axis. Life Sci., 2021, 272: 119232.
    [30]
    McCann J V, Liu A, Musante L, et al. A miRNA signature in endothelial cell-derived extracellular vesicles in tumor-bearing mice. Sci. Rep., 2019, 9(1): 16743.
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