Angiotensin II-induced muscle atrophy via PPARγ suppression is mediated by miR-29b.
Angiotensin II-induced muscle atrophy via PPARγ suppression is mediated by miR-29b.
复制标题
血管紧张素 II 通过 PPARγ 抑制诱导的肌肉萎缩是由 miR-29b 介导的
DOI：
10.1016/j.omtn.2020.12.015
复制
发表时间：
2021-03-05
期刊：
影响因子：
--
通讯作者：
Xiao J
中科院分区：
文献类型：
--
作者：
Li J;Yang T;Sha Z;Tang H;Hua X;Wang L;Wang Z;Gao Z;Sluijter JPG;Rowe GC;Das S;Yang L;Xiao J
血管紧张素II（AngII）水平升高诱导的肾素-血管紧张素系统（RAS）激活与肌肉萎缩有关，而肌肉萎缩与充血性心力衰竭的发病机制有关。虽然过氧化物酶体增殖物激活受体γ（PPARγ）激活可以抑制RAS，但PPARγ在AngII诱导的肌肉萎缩中的确切作用尚不清楚。在这里，我们确定了PPARγ作为miR-29 b的负调节因子，miR-29 b是一种能够促进多种类型肌肉萎缩的microRNA。抑制miR-29 b可以在体外和体内预防AngII诱导的肌肉萎缩。IGF 1、PI 3 K（p85α）和Yin Yang 1（YY 1）被确定为miR-29 b的靶基因，这些靶基因的过表达可以挽救AngII诱导的肌肉萎缩。重要的是，抑制PPARγ足以诱导肌肉萎缩，而PPARγ过表达可以减轻这种情况。这些数据表明，PPARγ/miR-29 b轴介导AngII诱导的肌肉萎缩，增加PPARγ或抑制miR-29 b代表了对抗AngII诱导的肌肉萎缩的有希望的方法。Xiao及其同事报道，PPARγ/miR-29 b轴通过抑制靶基因IGF 1、PI 3 K（p85α）和Yin Yang 1（YY 1）以及AKT/FOXO 3A/mTOR通路介导Ang II诱导的肌肉萎缩。他们的工作表明，过表达PPARγ和抑制miR-29 b是对抗AngII诱导的肌肉萎缩的新方法。
The activation of the renin-angiotensin system (RAS) induced by increased angiotensin II (AngII) levels has been implicated in muscle atrophy, which is involved in the pathogenesis of congestive heart failure. Although peroxisome proliferator-activated receptor gamma (PPARγ) activation can suppress RAS, the exact role of PPARγ in AngII-induced muscle atrophy is unclear. Here we identified PPARγ as a negative regulator of miR-29b, a microRNA that is able to promote multiple types of muscle atrophy. Suppression of miR-29b could prevent AngII-induced muscle atrophy both in vitro and in vivo. IGF1, PI3K(p85α), and Yin Yang 1 (YY1) were identified as target genes of miR-29b, and overexpression of these targets could rescue AngII-induced muscle atrophy. Importantly, inhibition of PPARγ was sufficient to induce muscle atrophy, while PPARγ overexpression could attenuate that. These data indicate that the PPARγ/miR-29b axis mediates AngII-induced muscle atrophy, and increasing PPARγ or inhibiting miR-29b represents a promising approach to counteract AngII-induced muscle atrophy. Xiao and colleagues report that the PPARγ/miR-29b axis mediates Ang II-induced muscle atrophy via inhibition of the target genes IGF1, PI3K(p85α), and Yin Yang 1 (YY1) and the AKT/FOXO3A/mTOR pathway. Their work implies that overexpression of PPARγ and inhibition of miR-29b are novel approaches to counteract AngII-induced muscle atrophy.
登录
查看更多内容
影响因子：
2.9
作者：
Chandra M;Miriyala S;Panchatcharam M
通讯作者：
Panchatcharam M
影响因子：
2.7
作者：
Malavaki, C. J.;Sakkas, G. K.;Karatzaferi, C.
通讯作者：
Karatzaferi, C.
影响因子：
5.5
作者：
Hudson, Matthew B.;Woodworth-Hobbs, Myra E.;Price, S. Russ
通讯作者：
Price, S. Russ
DOI：
10.18632/aging.101207
发表时间：
2017-03-22
期刊：
Aging
影响因子：
--
作者：
Pardo PS;Hajira A;Boriek AM;Mohamed JS
通讯作者：
Mohamed JS
影响因子：
20.1
作者：
Du Bois P;Pablo Tortola C;Lodka D;Kny M;Schmidt F;Song K;Schmidt S;Bassel-Duby R;Olson EN;Fielitz J
通讯作者：
Fielitz J