@article{8dbea848facf4e079490194b6c3ae917,
title = "Angiotensin II-induced muscle atrophy via PPAR gamma suppression is mediated by miR-29b",
abstract = "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.",
keywords = "angiotensin II, miR-29b, muscle atrophy, PPARγ",
author = "Jin Li and Tingting Yang and Zhao Sha and Haifei Tang and Xuejiao Hua and Lijun Wang and Zitong Wang and Ziyu Gao and Sluijter, \{Joost P.G.\} and Rowe, \{Glenn C.\} and Saumya Das and Liming Yang and Junjie Xiao",
note = "Funding Information: This work was supported by the grants from Innovation Program of Shanghai Municipal Education Commission ( 2017-01-07-00-09-E00042 to J.X.); National Key Research and Development Project ( 2018YFE0113500 to J.X.); National Natural Science Foundation of China ( 82020108002 , 81722008 , and 81911540486 to J.X. and 81900359 to J.L.); a grant from Science and Technology Commission of Shanghai Municipality ( 18410722200 and 17010500100 to J.X.); the “Dawn” Program of Shanghai Education Commission (19SG34 to J.X.); Shanghai Sailing Program ( 19YF1416400 to J.L.); “Chen Guang” project supported by Shanghai Municipal Education Commission and Shanghai Education Development Foundation ( 19CG45 to J.L.); and the National Institutes of Health (grants UH3 TR000901 and HL122547 to S.D.). J.P.G.S. is supported by Horizon2020 ERC-2016-COG EVICARE ( 725229 ), Technobeat ( 668724 ), and Vrienden UMC Utrecht. Funding Information: This work was supported by the grants from Innovation Program of Shanghai Municipal Education Commission (2017-01-07-00-09-E00042 to J.X.); National Key Research and Development Project (2018YFE0113500 to J.X.); National Natural Science Foundation of China (82020108002, 81722008, and 81911540486 to J.X. and 81900359 to J.L.); a grant from Science and Technology Commission of Shanghai Municipality (18410722200 and 17010500100 to J.X.); the ?Dawn? Program of Shanghai Education Commission (19SG34 to J.X.); Shanghai Sailing Program(19YF1416400 to J.L.); ?Chen Guang? project supported by Shanghai Municipal Education Commission and Shanghai Education Development Foundation (19CG45 to J.L.); and the National Institutes of Health (grants UH3 TR000901 and HL122547 to S.D.). J.P.G.S. is supported by Horizon2020 ERC-2016-COG EVICARE (725229), Technobeat (668724), and Vrienden UMC Utrecht., J.X. and L.Y. designed the study and instructed all experiments. J.X. drafted the manuscript. J.L, T.Y. Z.S. H.T. X.H. L.W. Z.W. and Z.G. performed the experiments and analyzed the data. J.P.G.S. G.C.R. and S.D. provided technical assistance and revised the manuscript. The authors declare no competing interests. Publisher Copyright: {\textcopyright} 2020 The Authors",
year = "2021",
month = mar,
day = "5",
doi = "10.1016/j.omtn.2020.12.015",
language = "English",
volume = "23",
pages = "743--756",
journal = "Molecular therapy. Nucleic acids",
issn = "2162-2531",
publisher = "Nature Publishing Group",
}