FAM114A1 influences cardiac pathological remodeling by regulating angiotensin II signaling.

ABSTRACT: Cardiac pathological remodeling, a primary contributor to heart failure (HF) and death, is an important target for HF therapy. However, the signaling pathways that govern cardiac remodeling are not fully elucidated. Here, we found that a functionally unannotated human myocardial infarction-associated (MI-associated) gene, family with sequence similarity 114 member A1 (FAM114A1), is induced in failing human and mouse hearts compared with nonfailing hearts. Homozygous KO of Fam114a1 (Fam114a1-/-) in the mouse genome reduces cardiomyocyte hypertrophy, inflammation, and cardiac fibrosis while restoring cardiac function in angiotensin II-induced (Ang II-induced) and MI-induced HF mouse models. Cardiac fibroblasts (CFs) exhibit the highest FAM114A1 expression among different cardiac cell types.

SUBMITTER: Subbaiah KCV 

PROVIDER: S-EPMC9310534 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature