ACE2 as a potential therapeutic target for pandemic COVID-19.
ACE2 as a potential therapeutic target for pandemic COVID-19.
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DOI：
10.1039/d0ra08228g
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发表时间：
2020-10-27
期刊：
影响因子：
3.9
通讯作者：
Thakur, Suman S.
中科院分区：
文献类型：
--
作者：
Chatterjee, Bhaswati;Thakur, Suman S.
SARS-CoV-2病毒通过降低宿主血管紧张素转换酶2(ACE2)的表达，通过ACE2受体入侵宿主。这破坏了ACE/Ang II/AT1R轴和ACE2/Ang(1-7)/mAs受体轴之间的动态平衡。因此，临床批准的药物包括：(I)血管紧张素转换酶(ACE)抑制剂，如卡托普利和依那普利，(Ii)血管紧张素受体阻滞剂(ARB)，如氯沙坦、坎地沙坦、奥美沙坦、阿奇沙坦、厄贝沙坦和替米沙坦，以及(Iii)ACE抑制剂与ARB的组合，如氯沙坦与赖诺普利和卡托普利与氯沙坦，以及(Iv)重组ACE2，在不同的医疗条件下激活ACE2的能力，包括高血压、炎症、心血管和肺部疾病。这些临床批准的药物被发现激活了在不同医学条件下下调的ACE2，包括高血压、炎症、心血管疾病、肾脏和肺部疾病。因此，这些药物可能会被重新用于重新激活新冠肺炎患者下调的血管紧张素转换酶2。这些药物可以单独或联合使用，作为预防和治疗SARS-CoV-2病毒的药物。SARS-CoV-2病毒通过降低宿主血管紧张素转换酶2(ACE2)的表达，通过ACE2受体入侵宿主。
SARS-CoV-2 virus invades the host through angiotensin-converting enzyme 2 (ACE2) receptors by decreasing the ACE2 expression of the host. This disturbs the dynamic equilibrium between the ACE/Ang II/AT1R axis and ACE2/Ang (1–7)/Mas receptor axis. Therefore, the clinically approved drugs belonging to (i) angiotensin converting enzyme (ACE) inhibitors such as captopril, and enalaprilat, (ii) angiotensin-receptor blockers (ARBs) such as losartan, candesartan, olmesartan, azilsartan, irbesartan, and telmisartan and (iii) the combination of ACE inhibitors and ARBs such as losartan with lisinopril and captopril with losartan, and (iv) recombinant ACE2, were studied for their ability to activate ACE2 in different medical conditions including hypertension, inflammation, cardiovascular, renal and lung diseases. These clinically approved drugs were found to activate ACE2 that had been downregulated in different medical conditions including hypertension, inflammation, cardiovascular, renal and lung diseases. Therefore, these drugs may be repurposed to re-activate the downregulated ACE2 of COVID-19 patients. These drugs either alone or in combination may be repurposed as prophylactics and therapeutics against SARS-CoV-2 virus. SARS-CoV-2 virus invades the host through angiotensin-converting enzyme 2 (ACE2) receptors by decreasing the ACE2 expression of the host.
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