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SARS-CoV-2 与肾素血管紧张素系统相互作用的临床意义:美国心脏病学会评论专题周报。

Clinical Implications of SARS-CoV-2 Interaction With Renin Angiotensin System: JACC Review Topic of the Week.

机构信息

Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York.

Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York.

出版信息

J Am Coll Cardiol. 2020 Jun 23;75(24):3085-3095. doi: 10.1016/j.jacc.2020.04.028. Epub 2020 Apr 16.

DOI:10.1016/j.jacc.2020.04.028
PMID:32305401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7161517/
Abstract

Severe acute respiratory-syndrome coronavirus-2 (SARS-CoV-2) host cell infection is mediated by binding to angiotensin-converting enzyme 2 (ACE2). Systemic dysregulation observed in SARS-CoV was previously postulated to be due to ACE2/angiotensin 1-7 (Ang1-7)/Mas axis downregulation; increased ACE2 activity was shown to mediate disease protection. Because angiotensin II receptor blockers, ACE inhibitors, and mineralocorticoid receptor antagonists increase ACE2 receptor expression, it has been tacitly believed that the use of these agents may facilitate viral disease; thus, they should not be used in high-risk patients with cardiovascular disease. Based on the anti-inflammatory benefits of the upregulation of the ACE2/Ang1-7/Mas axis and previously demonstrated benefits of lung function improvement in SARS-CoV infections, it has been hypothesized that the benefits of treatment with renin-angiotensin system inhibitors in SARS-CoV-2 may outweigh the risks and at the very least should not be withheld.

摘要

严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)宿主细胞感染是通过与血管紧张素转换酶 2(ACE2)结合介导的。以前推测 SARS-CoV 中观察到的全身失调是由于 ACE2/血管紧张素 1-7(Ang1-7)/Mas 轴下调引起的;增加 ACE2 活性被证明可以介导疾病保护。由于血管紧张素 II 受体阻滞剂、血管紧张素转换酶抑制剂和盐皮质激素受体拮抗剂增加 ACE2 受体表达,因此人们一直认为这些药物的使用可能会促进病毒疾病;因此,它们不应该在心血管疾病高危患者中使用。基于 ACE2/Ang1-7/Mas 轴上调的抗炎益处以及之前在 SARS-CoV 感染中证明的改善肺功能的益处,人们假设在 SARS-CoV-2 中使用肾素-血管紧张素系统抑制剂的治疗益处可能超过风险,至少不应被拒绝。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9216/7161517/5f4e5414b33a/gr2_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9216/7161517/8d01f727f34a/fx1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9216/7161517/6c9ad8bde983/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9216/7161517/8d01f727f34a/gr3_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9216/7161517/5f4e5414b33a/gr2_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9216/7161517/8d01f727f34a/fx1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9216/7161517/6c9ad8bde983/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9216/7161517/8d01f727f34a/gr3_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9216/7161517/5f4e5414b33a/gr2_lrg.jpg

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