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ACE2 的抗衰老作用是否与其在肾素-血管紧张素系统中的作用有关?——比较 ACE2 缺陷型、筑波高血压型和 Mas 缺陷型小鼠的衰老表型得出的发现。

Is the anti-aging effect of ACE2 due to its role in the renin-angiotensin system?-Findings from a comparison of the aging phenotypes of ACE2-deficient, Tsukuba hypertensive, and Mas-deficient mice.

机构信息

Department of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Department of Medical Science Technology, Faculty of Medical Science Technology, Morinomiya University of Medical Sciences, Osaka, Osaka, Japan.

出版信息

Hypertens Res. 2023 May;46(5):1210-1220. doi: 10.1038/s41440-023-01189-y. Epub 2023 Feb 14.

DOI:10.1038/s41440-023-01189-y
PMID:36788301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9925940/
Abstract

Angiotensin converting enzyme 2 (ACE2) functions as an enzyme that produces angiotensin 1-7 (A1-7) from angiotensin II (AII) in the renin-angiotensin system (RAS). We evaluated aging phenotypes, especially skeletal muscle aging, in ACE2 systemically deficient (ACE2 KO) mice and found that ACE2 has an antiaging function. The characteristic aging phenotype observed in ACE2 KO mice was not reproduced in mice deficient in the A1-7 receptor Mas or in Tsukuba hypertensive mice, a model of chronic AII overproduction, suggesting that ACE2 has a RAS-independent antiaging function. In this review, the results we have obtained and related studies on the aging regulatory mechanism mediated by RAS components will be presented and summarized. We evaluated the aging phenotype of ACE2 systemically deficient (ACE2 KO) mice, particularly skeletal muscle aging, and found that ACE2 has an antiaging function. The characteristic aging phenotype observed in ACE2 KO mice was not reproduced in Mas KO mice, angiotensin 1-7 receptor-deficient mice or in Tsukuba hypertensive mice, a model of chronic angiotensin II overproduction, suggesting that the antiaging functions of ACE2 are independent of the renin-angiotensin system (RAS).

摘要

血管紧张素转换酶 2(ACE2)作为一种酶,在肾素-血管紧张素系统(RAS)中可将血管紧张素 II(AII)转化为血管紧张素 1-7(A1-7)。我们评估了 ACE2 系统缺乏(ACE2 KO)小鼠的衰老表型,特别是骨骼肌衰老,发现 ACE2 具有抗衰老功能。在 ACE2 KO 小鼠中观察到的特征性衰老表型在 A1-7 受体 Mas 缺乏或 Tsukuba 高血压小鼠(慢性 AII 过度产生的模型)中没有重现,这表明 ACE2 具有 RAS 独立的抗衰老功能。在这篇综述中,我们将介绍和总结 ACE2 介导的 RAS 成分调节衰老机制的相关研究结果。我们评估了 ACE2 系统缺乏(ACE2 KO)小鼠的衰老表型,特别是骨骼肌衰老,发现 ACE2 具有抗衰老功能。在 ACE2 KO 小鼠中观察到的特征性衰老表型在 Mas KO 小鼠、血管紧张素 1-7 受体缺乏小鼠或 Tsukuba 高血压小鼠(慢性血管紧张素 II 过度产生的模型)中没有重现,这表明 ACE2 的抗衰老功能独立于肾素-血管紧张素系统(RAS)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a51/9925940/24495dcd2b47/41440_2023_1189_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a51/9925940/2fb66e0fa73c/41440_2023_1189_Figa_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a51/9925940/6cbd414f803f/41440_2023_1189_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a51/9925940/0750b0cc0318/41440_2023_1189_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a51/9925940/24495dcd2b47/41440_2023_1189_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a51/9925940/2fb66e0fa73c/41440_2023_1189_Figa_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a51/9925940/6cbd414f803f/41440_2023_1189_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a51/9925940/0750b0cc0318/41440_2023_1189_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a51/9925940/24495dcd2b47/41440_2023_1189_Fig3_HTML.jpg

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