血管紧张素转换酶2在动脉粥样硬化中的研究进展

潘红波; 李明杰; 满雨楠; 陈罡

doi:10.13201/j.issn.1001-1439.2023.12.013

血管紧张素转换酶2在动脉粥样硬化中的研究进展

- 1.
  广西医科大学第一附属医院病理科(南宁，530021)
- 2.
  广西医科大学第一临床医学院法医学系
基金项目:
广西壮族自治区卫生健康委员会自筹经费科研项目(No：Z-A20220405、Z-A20220404)

详细信息

通讯作者: 陈罡，E-mail：chengang@gxmu.edu.cn

中图分类号: R541

收稿日期: 2022-12-15

刊出日期: 2023-12-13

Progress in angiotensin converting enzyme 2 in atherosclerosis

- 1.
  Department of Pathology, the First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China
- 2.
  Department of Forensic Medicine, the First Clinical School of Guangxi Medical University

More Information

Corresponding author: CHEN Gang, E-mail: chengang@gxmu.edu.cn

Received Date: 15 December 2022

Publish Date: 13 December 2023

摘要

摘要: 血管紧张素转换酶2(ACE2)在人体组织中普遍存在，特别是心血管系统。ACE2的生理功能之一是将血管紧张素-Ⅱ(Ang-Ⅱ)转化为血管紧张素1~7(Ang-1~7)，并在抑制动脉粥样硬化的形成中起到关键作用，但是单凭这一学说无法完全揭示其背后的作用机制，有必要从更多的角度去深入了解ACE2。因此本文就ACE2在动脉粥样硬化中的研究进展作一综述。
- 血管紧张素转换酶 /
- 动脉粥样硬化 /
- 非编码RNA
Abstract: Angiotensin converting enzyme 2(ACE2) is ubiquitously expressed in human tissues, particularly in the cardiovascular system. The one of physiological function of ACE2 is mainly to convert angiotensin II(Ang-II) into angiotensin 1-7(Ang-1-7) and plays a key role in inhibiting atherosclerosis. However, the mechanisms behind cannot be fully revealed by this doctrine alone. So it is necessary to gain insight into ACE2 from more perspectives. This review will focus on the recent progress of ACE2 in atherosclerosis.
- angiotensin-converting enzyme 2 /
- atherosclerosis /
- non-coding RNA

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图 1 ACE2在动脉粥样硬化中作用示意图

Figure 1. ACE2 in atherosclerosis

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参考文献(51)

[1]	Roth GA, MeNSAH GA, Johnson CO, et al. Global burden of cardiovascular diseases and risk factors, 1990-2019: Update From the GBD 2019 Study[J]. J Am Coll Cardiol, 2020, 76(25): 2982-3021. doi: 10.1016/j.jacc.2020.11.010
[2]	Jebari-Benslaiman S, Galicia-García U, Larrea-Sebal A, et al. Pathophysiology of Atherosclerosis[J]. Int J Mol Sci, 2022, 23(6): 110.
[3]	Mogi M. Effect of renin-angiotensin system on senescence[J]. Geriatr Gerontol Int, 2020, 20(6): 520-525. doi: 10.1111/ggi.13927
[4]	Gheblawi M, Wang K, Viveiros A, et al. Angiotensin-Converting Enzyme 2: SARS-CoV-2 Receptor and Regulator of the Renin-Angiotensin System: Celebrating the 20th Anniversary of the Discovery of ACE2[J]. Circ Res, 2020, 126(10): 1456-1474. doi: 10.1161/CIRCRESAHA.120.317015
[5]	Poznyak AV, Bezsonov EE, Eid AH, et al. ACE2 Is an Adjacent Element of Atherosclerosis and COVID-19 Pathogenesis[J]. Int J Mol Sci, 2021, 22(9): 110.
[6]	Bhushan S, Xiao Z, Gao K, et al. Role and Interaction Between ACE1, ACE2 and Their Related Genes in Cardiovascular Disorders[J]. Curr Probl Cardiol, 2023, 48(8): 101162. doi: 10.1016/j.cpcardiol.2022.101162
[7]	Liao W, Wu J. The ACE2/Ang(1-7)/MasR axis as an emerging target for antihypertensive peptides[J]. Crit Rev Food Sci Nutr, 2021, 61(15): 2572-2586. doi: 10.1080/10408398.2020.1781049
[8]	Silva GM, França-Falcão MS, Calzerra N, et al. Role of renin-angiotensin system components in atherosclerosis: focus on Ang-Ⅱ, ACE2, and Ang-1-7[J]. Front Physiol, 2020, 11: 1067. doi: 10.3389/fphys.2020.01067
[9]	Li Z, Wang K, Ji X, et al. ACE2 suppresses the inflammatory response in LPS-induced porcine intestinal epithelial cells via regulating the NF-κB and MAPK pathways[J]. Peptides, 2022, 149: 170717. doi: 10.1016/j.peptides.2021.170717
[10]	Djomkam A, Olwal CO, Sala TB, et al. Commentary: SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor[J]. Front Oncol, 2020, 10: 1448. doi: 10.3389/fonc.2020.01448
[11]	Fan J, Watanabe T. Atherosclerosis: Known and unknown[J]. Pathol Int, 2022, 72(3): 151-160. doi: 10.1111/pin.13202
[12]	Jung SH, Lee KT. Atherosclerosis by Virus Infection-A Short Review[J]. Biomedicines, 2022, 10(10): 110.
[13]	Ranković I, Milivojević V, Pavlović Marković A, et al. Interplay between chronic hepatitis B and atherosclerosis: Innovative perspectives and theories[J]. World J Gastroenterol, 2022, 28(4): 497-499. doi: 10.3748/wjg.v28.i4.497
[14]	Shi Y, Tokunaga O. Herpesvirus(HSV-1, EBV and CMV)infections in atherosclerotic compared with non-atherosclerotic aortic tissue[J]. Pathol Int, 2002, 52(1): 31-39. doi: 10.1046/j.1440-1827.2002.01312.x
[15]	Wu YP, Sun DD, Wang Y, et al. Herpes Simplex Virus Type 1 and Type 2 Infection Increases Atherosclerosis Risk: Evidence Based on a Meta-Analysis[J]. Biomed Res Int, 2016, 2016: 2630865.
[16]	Lo J, Abbara S, Shturman L, et al. Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men[J]. AIDS, 2010, 24(2): 243-253. doi: 10.1097/QAD.0b013e328333ea9e
[17]	Liu Y, Zhang HG. Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection[J]. Front Med(Lausanne), 2020, 7: 629413.
[18]	Zheng YY, Ma YT, Zhang JY, et al. COVID-19 and the cardiovascular system[J]. Nat Rev Cardiol, 2020, 17(5): 259-260. doi: 10.1038/s41569-020-0360-5
[19]	Tabas I, Lichtman AH. Monocyte-Macrophages and T Cells in Atherosclerosis[J]. Immunity, 2017, 47(4): 621-634. doi: 10.1016/j.immuni.2017.09.008
[20]	Sima P, Vannucci L, Vetvicka V. Atherosclerosis as autoimmune disease[J]. Ann Transl Med, 2018, 6(7): 116. doi: 10.21037/atm.2018.02.02
[21]	Vinciguerra M, Romiti S, Fattouch K, et al. Atherosclerosis as Pathogenetic Substrate for Sars-Cov2 Cytokine Storm[J]. J Clin Med, 2020, 9(7): 110.
[22]	Vassiliou AG, Zacharis A, Keskinidou C, et al. Soluble Angiotensin Converting Enzyme 2(ACE2) Is Upregulated and Soluble Endothelial Nitric Oxide Synthase(eNOS)Is Downregulated in COVID-19-induced Acute Respiratory Distress Syndrome(ARDS)[J]. Pharmaceuticals(Basel), 2021, 14(7): 110.
[23]	Zhang Y, Yan R, Zhou Q. ACE2, B0AT1, and SARS-CoV-2 spike protein: Structural and functional implications[J]. Curr Opin Struct Biol, 2022, 74: 102388. doi: 10.1016/j.sbi.2022.102388
[24]	Wang J, Zhao H, An Y. ACE2 Shedding and the Role in COVID-19[J]. Front Cell Infect Microbiol, 2021, 11: 789180.
[25]	Sardu C, Gambardella J, Morelli MB, et al. Hypertension, Thrombosis, Kidney Failure, and Diabetes: Is COVID-19 an Endothelial Disease? A Comprehensive Evaluation of Clinical and Basic Evidence[J]. J Clin Med, 2020, 9(5): 110.
[26]	Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19[J]. N Engl J Med, 2020, 383(2): 120-128. doi: 10.1056/NEJMoa2015432
[27]	Varga Z, Flammer AJ, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19[J]. Lancet, 2020, 395(10234): 1417-1418. doi: 10.1016/S0140-6736(20)30937-5
[28]	Colmenero I, Santonja C, Alonso-Riaño M, et al. SARS-CoV-2 endothelial infection causes COVID-19 chilblains: histopathological, immunohistochemical and ultrastructural study of seven paediatric cases[J]. Br J Dermatol, 2020, 183(4): 729-737. doi: 10.1111/bjd.19327
[29]	Monteil V, Kwon H, Prado P, et al. Inhibition of SARS-CoV-2 Infections in Engineered Human Tissues Using Clinical-Grade Soluble Human ACE2[J]. Cell, 2020, 181(4): 905-913.e7. doi: 10.1016/j.cell.2020.04.004
[30]	Klh fek J. The role of angiotensin-converting enzyme 2 in the pathogenesis of COVID-19: the villain or the hero?[J]. Acta Clin Belg, 2022, 77(1): 211-218. doi: 10.1080/17843286.2020.1786324
[31]	Panni S, Lovering RC, Porras P, et al. Non-coding RNA regulatory networks[J]. Biochim Biophys Acta Gene Regul Mech, 2020, 1863(6): 194417. doi: 10.1016/j.bbagrm.2019.194417
[32]	Gu Q, Wang B, Zhang XF, et al. Contribution of renin-angiotensin system to exercise-induced attenuation of aortic remodeling and improvement of endothelial function in spontaneously hypertensive rats[J]. Cardiovasc Pathol, 2014, 23(5): 298-305. doi: 10.1016/j.carpath.2014.05.006
[33]	Yang JM, Dong M, Meng X, et al. Angiotensin-(1-7) dose-dependently inhibits atherosclerotic lesion formation and enhances plaque stability by targeting vascular cells[J]. Arterioscler Thromb Vasc Biol, 2013, 33(8): 1978-1985. doi: 10.1161/ATVBAHA.113.301320
[34]	Wang HJ, Lo WY, Lin LJ. Angiotensin-(1-7) decreases glycated albumin-induced endothelial interleukin-6 expression via modulation of miR-146a[J]. Biochem Biophys Res Commun, 2013, 430(3): 1157-1163. doi: 10.1016/j.bbrc.2012.12.018
[35]	Trojanowicz B, Imdahl T, Ulrich C, et al. Circulating miR-421 Targeting Leucocytic Angiotensin Converting Enzyme 2 Is Elevated in Patients with Chronic Kidney Disease[J]. Nephron, 2019, 141(1): 61-74. doi: 10.1159/000493805
[36]	尹亮, 甘露, 史博群等. 长链非编码RNA在冠状动脉慢性完全闭塞病变的应用展望[J]. 临床心血管病杂志, 2021, 37(2): 172-127. doi: 10.13201/j.issn.1001-1439.2021.02.017
[37]	Josefs T, Boon RA. The Long Non-coding Road to Atherosclerosis[J]. Curr Atheroscler Rep, 2020, 22(10): 55. doi: 10.1007/s11883-020-00872-6
[38]	Khyzha N, Khor M, DiStefano PV, et al. Regulation of CCL2 expression in human vascular endothelial cells by a neighboring divergently transcribed long noncoding RNA[J]. Proc Natl Acad Sci U S A, 2019, 116(33): 16410-16419. doi: 10.1073/pnas.1904108116
[39]	Li W, Wang R, Ma JY, et al. A Human Long Non-Coding RNA ALT1 Controls the Cell Cycle of Vascular Endothelial Cells Via ACE2 and Cyclin D1 Pathway[J]. Cell Physiol Biochem, 2017, 43(3): 1152-1167. doi: 10.1159/000481756
[40]	Ferns G, Heikal L. Hypoxia in Atherogenesis[J]. Angiology, 2017, 68(6): 472-493. doi: 10.1177/0003319716662423
[41]	Yu Z, Huang Q, Zhang Q, et al. CircRNAs open a new era in the study of cardiovascular disease(Review)[J]. Int J Mol Med, 2021, 47(1): 49-64.
[42]	Si X, Zheng H, Wei G, et al. circRNA Hipk3 Induces Cardiac Regeneration after Myocardial Infarction in Mice by Binding to Notch1 and miR-133a[J]. Mol Ther Nucleic Acids, 2020, 21: 636-655. doi: 10.1016/j.omtn.2020.06.024
[43]	Bao MH, Zhang RQ, Huang XS, et al. Transcriptomic and Proteomic Profiling of Human Stable and Unstable Carotid Atherosclerotic Plaques[J]. Front Genet, 2021, 12: 755507. doi: 10.3389/fgene.2021.755507
[44]	Arora S, Singh P, Dohare R, et al. Unravelling host-pathogen interactions: ceRNA network in SARS-CoV-2 infection(COVID-19)[J]. Gene, 2020, 762: 145057. doi: 10.1016/j.gene.2020.145057
[45]	Ahmadi Badi S, Malek A, Paolini A, et al. Downregulation of ACE, AGTR1, and ACE2 genes mediating SARS-CoV-2 pathogenesis by gut microbiota members and their postbiotics on Caco-2 cells[J]. Microb Pathog, 2022, 173(Pt A): 105798.
[46]	Cretoiu D, Ionescu RF, Enache RM, et al. Gut Microbiome, Functional Food, Atherosclerosis, and Vascular Calcifications-Is There a Missing Link?[J]. Microorganisms, 2021, 9(9): 110.
[47]	高中山, 任明. 短链脂肪酸在冠心病防治中的研究进展[J]. 临床心血管病杂志, 2021, 37(11): 1062-1066. https://lcxxg.whuhzzs.com/article/doi/10.13201/j.issn.1001-1439.2021.11.019
[48]	Anselmi G, Gagliardi L, Egidi G, et al. Gut microbiota and cardiovascular diseases: a critical review[J]. Cardiol Rev, 2021, 29(4): 195-204. doi: 10.1097/CRD.0000000000000327
[49]	Witkowski M, Weeks TL, Hazen SL. Gut microbiota and cardiovascular disease[J]. Circ Res, 2020, 127(4): 553-570. doi: 10.1161/CIRCRESAHA.120.316242
[50]	Sudar-Milovanovic E, Gluvic Z, Obradovic M, et al. Tryptophan metabolism in atherosclerosis and diabetes[J]. Curr Med Chem, 2022, 29(1): 99-113. doi: 10.2174/0929867328666210714153649
[51]	Camargo SM, Singer D, Makrides V, et al. Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations[J]. Gastroenterology, 2009, 136(3): 872-82. doi: 10.1053/j.gastro.2008.10.055