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. 2021 Aug 26;9:666422. doi: 10.3389/fcell.2021.666422

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Copyright © 2021 Xie, Yao, Hu, Cai, Zhao, Yuan, Wu and Tang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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High-mobility group A1 (HMGA1) knockdown alleviated cardiac fibrosis and dysfunction induced by angiotensin II (Ang II) in mice. (A) The protein level of HMGA1 in mouse hearts 3 weeks after AAV9-shHMGA1 injection (n = 6). (B) Immunofluorescence staining of HMGA1 and α-SMA in heart tissue post-AAV9-shHMGA1 injection and Ang II infusion (n = 5). (C) PSR staining image and quantitative result of left ventricular collagen volume in mouse hearts 28 days after Ang II infusion (n = 5). (D) Transcription levels of collagen I, collagen III, and TGFβ1 (n = 6). (E) Protein levels of collagen III and α-SMA in heart tissue (n = 6). (F) Echocardiographic results in each group (n = 10). *p < 0.05.