血管内皮细胞功能障碍在慢性非传染性疾病发病中的病理作用

刘志兵; 朱启星

doi:10.19837/j.cnki.ahyf.2021.06.002

PDF(918 KB)

安徽预防医学杂志 ›› 2021, Vol. 27 ›› Issue (6) : 422-428. DOI: 10.19837/j.cnki.ahyf.2021.06.002

专家约稿

血管内皮细胞功能障碍在慢性非传染性疾病发病中的病理作用

刘志兵, 朱启星

作者信息 +

The role of vascular endothelial cell dysfunction in chronic non-communicable diseases

LIU Zhi-bing, ZHU Qi-xing

Author information +

文章历史 +

摘要

目的血管内皮细胞是机体最大的内分泌组织细胞,位于血流与血管壁之间,将血液与血管壁分离开来。血管内皮细胞通过合成和释放多种内皮源性舒张因子和收缩因子在调节血管张力方面发挥着重要作用。此外,内皮细胞在维持抗凝/促凝平衡、血管生成、内分泌以及炎症和免疫中的作用也越来越被重视。越来越多的证据表明,血管内皮细胞功能对血管内稳态的维持至关重要,血管内皮细胞功能障碍是与血管收缩、血栓形成和炎症状态有关的各种微血管病变相关疾病的共同标志。本文主要就血管内皮细胞的结构和功能,以及功能障碍在心血管疾病、糖尿病并发症、慢性肾病等慢性非传染性疾病中的作用进行综述。

Abstract

Objective Vascular endothelial cells are the largest endocrine tissue cells in the body.They are located between the blood stream and the vessel wall and separate the blood from the vessel wall.Vascular endothelial cells play an important role in regulating vascular tension by synthesizing and releasing a variety of endothelial-derived vasodilator and vasoconstrictor factors.In addition,more and more attention has been paid to the role of vascular endothelial cells in maintaining anticoagulation/procoagulation balance,angiogenesis,endocrine,inflammation and immunity.Increasing number of evidences show that vascular endothelial cells function is essential for the maintenance of vascular homeostasis.Vascular endothelial cells dysfunction is a common sign of various microvascular diseases related to vasoconstriction,thrombosis and inflammation.This article mainly reviews the structure and function of vascular endothelial cells,as well as the role of dysfunction in chronic non-communicable diseases such as cardiovascular disease,diabetic complications,and chronic kidney disease.

导出引用

刘志兵, 朱启星. 血管内皮细胞功能障碍在慢性非传染性疾病发病中的病理作用[J]. 安徽预防医学杂志. 2021, 27(6): 422-428 https://doi.org/10.19837/j.cnki.ahyf.2021.06.002

LIU Zhi-bing, ZHU Qi-xing. The role of vascular endothelial cell dysfunction in chronic non-communicable diseases[J]. Anhui Journal of Preventive Medicine. 2021, 27(6): 422-428 https://doi.org/10.19837/j.cnki.ahyf.2021.06.002

中图分类号： R195.4

参考文献

[1] Sturtzel C.Endothelial Cells[J].Adv Exp Med Biol,2017,1003:71-91.
[2] Siragusa M,Fleming I.The eNOS signalosome and its link to endothelial dysfunction[J].Pflugers Arch,2016,468(7):1125-1137.
[3] Chistiakov DA,Orekhov AN,Bobryshev YV.Effects of shear stress on endothelial cells: go with the flow[J].Acta Physiol (Oxf),2017,219(2):382-408.
[4] Cyr AR,Huckaby LV,Shiva SS,Zuckerbraun BS.Nitric Oxide and Endothelial Dysfunction[J].Crit Care Clin,2020,36(2):307-321.
[5] Engelmann B,Massberg S.Thrombosis as an intravascular effector of innate immunity[J].Nat Rev Immunol,2013,13(1):34-45.
[6] Davenport AP,Hyndman KA,Dhaun N,et al.Endothelin[J].Pharmacol Rev,2016,68(2):357-418.
[7] Blanco R,Gerhardt H.VEGF and Notch in tip and stalk cell selection[J].Cold Spring Harb Perspect Med,2013,3(1):a006569.
[8] Khakpour S,Wilhelmsen K,Hellman J.Vascular endothelial cell Toll-like receptor pathways in sepsis[J].Innate Immun,2015,21(8):827-846.
[9] Carambia A,Frenzel C,Bruns OT,et al.Inhibition of inflammatory CD4 T cell activity by murine liver sinusoidal endothelial cells[J].J Hepatol,2013,58(1):112-118.
[10] GBD 2017 Causes of Death Collaborators.Global,regional,and national age-sex-specific mortality for 282 causes of death in 195 countries and territories,1980-2017: a systematic analysis for the Global Burden of Disease Study 2017[J].Lancet,2018,392(10159):1736-1788.
[11] Cybulsky MI,Gimbrone MA Jr.Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis[J].Science,1991,251(4995):788-791.
[12] De Caterina R,Basta G,Lazzerini G,et al.Soluble vascular cell adhesion molecule-1 as a biohumoral correlate of atherosclerosis[J].Arterioscler Thromb Vasc Biol,1997,17(11):2646-2654.
[13] Cybulsky MI,Iiyama K,Li H,et al.A major role for VCAM-1,but not ICAM-1,in early atherosclerosis[J].J Clin Invest,2001,107(10):1255-1262.
[14] Simion V,Zhou H,Pierce JB,et al.LncRNAVINAS regulates atherosclerosis by modulating NF-κB and MAPK signaling[J].JCI Insight,2020,5(21):e140627.
[15] Zhong L,Simard MJ,Huot J.Endothelial microRNAs regulating the NF-κB pathway and cell adhesion molecules during inflammation[J].FASEB J,2018,32(8):4070-4084.
[16] Gimbrone MA Jr,García-Cardeña G.Vascular endothelium,hemodynamics,and the pathobiology of atherosclerosis[J].Cardiovasc Pathol,2013,22(1):9-15.
[17] Parmar KM,Larman HB,Dai G,et al.Integration of flow-dependent endothelial phenotypes byKruppel-like factor 2[J].J Clin Invest,2006,116(1):49-58.
[18] Zhuang T,Liu J,Chen X,et al.Endothelial Foxp1 Suppresses Atherosclerosis via Modulation of Nlrp3 Inflammasome Activation[J].Circ Res,2019,125(6):590-605.
[19] Atkins GB,Wang Y,Mahabeleshwar GH,et al.Hemizygous deficiency of Krüppel-like factor 2 augments experimental atherosclerosis[J].Circ Res,2008,103(7):690-693.
[20] Fan W,Fang R,Wu X,et al.Shear-sensitivemicroRNA-34a modulates flow-dependent regulation of endothelial inflammation[J].J Cell Sci,2015,128(1):70-80.
[21] Dunn J,Thabet S,Jo H.Flow-Dependent Epigenetic DNA Methylation in Endothelial Gene Expression and Atherosclerosis[J].Arterioscler Thromb Vasc Biol,2015,35(7):1562-1569.
[22] Moonen JR,Lee ES,Schmidt M,et al.Endothelial-to-mesenchymal transition contributes to fibro-proliferative vascular disease and is modulated by fluid shear stress[J].Cardiovasc Res,2015,108(3):377-386.
[23] Mahmoud MM,Serbanovic-Canic J,Feng S,et al.Shear stress induces endothelial-to-mesenchymal transition via the transcription factor Snail[J].Sci Rep,2017,7(1):3375.
[24] Chen PY,Qin L,Baeyens N,et al.Endothelial-to-mesenchymal transition drives atherosclerosis progression[J].J Clin Invest,2015,125(12):4514-4528.
[25] Marques FK,Campos FM,Sousa LP,Teixeira-Carvalho A,Dusse LM,Gomes KB.Association of microparticles and preeclampsia[J].Mol Biol Rep,2013,40(7):4553-4559.
[26] Zhang JR,Sun HJ.LncRNAs and circular RNAs as endothelial cell messengers in hypertension: mechanism insights and therapeutic potential[J].Mol Biol Rep,2020,47(7):5535-5547.
[27] Deckert T,Feldt-Rasmussen B,Borch-Johnsen K,Jensen T,Kofoed-Enevoldsen A.Albuminuria reflects widespread vascular damage[J].The Steno hypothesis,Diabetologia,1989;32(4):219-226.
[28] Kumar Vr S,Darisipudi MN,Steiger S,et al.Cathepsin S Cleavage of Protease-Activated Receptor-2 on Endothelial Cells Promotes Microvascular Diabetes Complications[J].J Am Soc Nephrol,2016,27(6):1635-1649.
[29] Gilbert RE.The endothelium in diabetic nephropathy[J].Curr Atheroscler Rep,2014,16(5):410.
[30] Majumder S,Advani A.VEGF and the diabetic kidney: More than too much of a good thing[J].J Diabetes Complications,2017,31(1):273-279.
[31] Cheng H,Harris RC.Renal endothelial dysfunction in diabetic nephropathy[J].Cardiovasc Hematol Disord Drug Targets,2014,14(1):22-33.
[32] Garsen M,Lenoir O,Rops AL,et al.Endothelin-1 Induces Proteinuria by Heparanase-Mediated Disruption of the Glomerular Glycocalyx[J].J Am Soc Nephrol,2016,27(12):3545-3551.
[33] Rabelink TJ,van den Berg BM,Garsen M,Wang G,Elkin M,van der Vlag J.Heparanase: roles in cell survival,extracellular matrix remodelling and the development of kidney disease[J].Nat Rev Nephrol,2017,13(4):201-212.
[34] Hu T,Shi JJ,Fang J,Wang Q,Chen YB,Zhang SJ.Quercetin ameliorates diabetic encephalopathy through SIRT1/ER stress pathway in db/db mice[J].Aging (Albany NY),2020,12(8):7015-7029.
[35] Goligorsky MS.Vascular endothelium in diabetes[J].Am J Physiol Renal Physiol,2017,312(2):F266-F275.
[36] Hubbard BP,Sinclair DA.Small molecule SIRT1 activators for the treatment of aging and age-related diseases[J].Trends Pharmacol Sci,2014,35(3):146-154.
[37] Chen J,Xavier S,Moskowitz-Kassai E,et al.Cathepsin cleavage of sirtuin 1 in endothelial progenitor cells mediates stress-induced premature senescence[J].Am J Pathol,2012,180(3):973-983.
[38] Tao D,Ni N,Zhang T,et al.Accumulation of advanced glycation end products potentiate human retinal capillary endothelial cells mediated diabetic retinopathy[J].Mol Med Rep,2019,20(4):3719-3727.
[39] Chhabra M,Sharma S.Potential role of Peroxisome Proliferator Activated Receptor gamma analogues in regulation of endothelial progenitor cells in diabetes mellitus: An overview[J].Diabetes Metab Syndr,2019,13(2):1123-1129.
[40] Masuda T,Shimazawa M,Hara H.RetinalDiseases Associated with Oxidative Stress and the Effects of a Free Radical Scavenger (Edaravone)[J].Oxid Med Cell Longev,2017,2017:9208489.
[41] Wooff Y,Man SM,Aggio-Bruce R,Natoli R,Fernando N.IL-1 Family Members Mediate Cell Death,Inflammation and Angiogenesis in Retinal Degenerative Diseases[J].Front Immunol,2019,10:1618.
[42] Taghavi Y,Hassanshahi G,Kounis NG,Koniari I,Khorramdelazad H.Monocyte chemoattractant protein-1 (MCP-1/CCL2) in diabetic retinopathy: latest evidence and clinical considerations[J].J Cell Commun Signal,2019,13(4):451-462.
[43] Dumas E,Neagoe PE,McDonald PP,White M,Sirois MG.New Insights into the Pro-Inflammatory Activities of Ang1 on Neutrophils: Induction of MIP-1β Synthesis and Release[J].PLoS One,2016,11(9):e0163140.
[44] Khalfaoui T,Lizard G,Ouertani-Meddeb A.Adhesion molecules (ICAM-1 and VCAM-1) and diabetic retinopathy in type 2 diabetes[J].J Mol Histol,2008,39(2):243-249.
[45] Rezk NA,Sabbah NA,Saad MS.Role of MicroRNA 126 in screening,diagnosis,and prognosis of diabetic patients in Egypt[J].IUBMB Life,2016,68(6):452-458.
[46] Eloueyk A,Osta B,Alameldinne R,Awad D.Uremic Serum Induces Inflammation in Cultured Human Endothelial Cells and Triggers Vascular Repair Mechanisms[J].Inflammation,2019,42(6):2003-2010.
[47] Serradell M,Díaz-Ricart M,Cases A,et al.Uremic medium causes expression,redistribution and shedding of adhesion molecules in cultured endothelial cells[J].Haematologica,2002,87(10):1053-1061.
[48] Shang F,Wang SC,Hsu CY,et al.MicroRNA-92a Mediates Endothelial Dysfunction in CKD[J].J Am Soc Nephrol,2017,28(11):3251-3261.
[49] Addi T,Dou L,Burtey S.Tryptophan-Derived Uremic Toxins and Thrombosis in Chronic Kidney Disease[J].Toxins (Basel),2018,10(10):412.
[50] Soriano S,Carmona A,Triviño F,et al.Endothelial damage and vascular calcification in patients with chronic kidney disease[J].Am J Physiol Renal Physiol,2014,307(11):F1302-F1311.
[41] Gao C,Xie R,Yu C,et al.Thrombotic Role of Blood and Endothelial Cells in Uremia through Phosphatidylserine Exposure and Microparticle Release[J].PLoS One,2015,10(11):e0142835.
[52] Takatori H,Makita S,Ito T,Matsuki A,Nakajima H.Regulatory Mechanisms of IL-33-ST2-Mediated Allergic Inflammation[J].Front Immunol,2018,9:2004.
[53] Laumonnier Y,Wiese AV,Figge J,Karsten C.Regulation and function of anaphylatoxins and their receptors in allergic asthma[J].Mol Immunol,2017,84:51-56.
[54] Jiao A,Fish SC,Mason LE,Schelling SH,Goldman SJ,Williams CM.A role for endothelial selectins in allergic and nonallergic inflammatory disease[J].Ann Allergy Asthma Immunol,2007,98(1):83-88.
[55] García-Vicuña R,Gómez-Gaviro MV,Domínguez-Luis MJ,et al.CC and CXC chemokine receptors mediate migration,proliferation,and matrix metalloproteinase production by fibroblast-like synoviocytes fromrheumatoid arthritis patients[J].Arthritis Rheum,2004,50(12):3866-3877.
[56] Tornero Molina J,Balsa Criado A,Blanco García F,et al.Expert Recommendations on the Interleukin 6 Blockade in Patients with Rheumatoid Arthritis.Recomendaciones de experto sobre el bloqueo de la interleucina 6 en pacientes con artritis reumatoide[J].Reumatol Clin (Engl Ed),2020,16(4):272-281.
[57] Wang DG,Tang XW,Fan Y,et al.Decreased flow-mediated dilatation in patients with systemic lupus erythematosus: a meta-analysis[J].Inflammation,2014,37(6):2067-2075.