Correlation Engine 2.0
Clear Search sequence regions

Sizes of these terms reflect their relevance to your search.

Autophagy suppression plays key a role during myocardial fibrosis (MF) progression. Exosomes from stem cells attenuate MF. The current study aimed to explain the antifibrosis effects of exosomes by focusing on microRNAs (miRs). MF was induced in rats using transverse aortic constriction (TAC) method and handled with exosomes from bone mesenchymal stem cells (BMSCs). The results of in vivo assays were verified with H9c2 cells. MiR expression profile was determined using microarray detection. The influence of miR-199a-3p modulation in vivo and in vitro on the antifibrosis effect of exosomes then was assessed. Exosomes attenuated MF by inhibiting inflammation, improving tissue structure, and inhibiting fibrosis-related indicators in TAC rats, and the effects were associated with autophagy activation. In H9c2 cells, exosomes suppressed cell viability, induced cell apoptosis, inhibited fibrosis-related indicators, while and the inhibition of autophagy by 3-MA would block the effect of exosomes. Based on the microarray detection, miR-199a-3p level was selected as therapeutic target. The inhibition of miR-199a-3p impaired the antifibrosis effects of exosomes on H9c2 cells, which was associated with autophagy inhibition. Collectively, exosomes from BMSCs exerted antifibrosis effects via the distant transfer of miR-199a-3p to heart tissues, which induced autophagy by inhibiting mTOR. © 2022. The Author(s) under exclusive licence to Japan Human Cell Society.


Chenrong Fan, Qizeng Wang, Youjin Chen, Tingting Ye, Yuncao Fan. Exosomes derived from bone mesenchymal stem cells attenuate myocardial fibrosis both in vivo and in vitro via autophagy activation: the key role of miR-199a-3p/mTOR pathway. Human cell. 2022 May;35(3):817-835

Expand section icon Mesh Tags

Expand section icon Substances

PMID: 35190954

View Full Text