ANO1 relieves pressure overload-induced myocardial fibrosis in mice by inhibiting TGF- β/Smad3 signaling pathway.

CONCLUSIONS: In the case of cardiac pressure overload in mice, ANO1 is lowly expressed in myocardial tissues. Meanwhile, its overexpression is able to attenuate pressure overload-induced myocardial fibrosis in mice by repressing the TGF-β/smad3 signaling pathway. All our findings indicate that ANO1 can serve as a potential gene target for the treatment of myocardial fibrosis in the future. PMID: 32894555 [PubMed - as supplied by publisher]
Source: European Review for Medical and Pharmacological Sciences - Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research