Inhibition of miR-25 Ameliorates Cardiac Dysfunction and Fibrosis by Restoring Kruppel-like Factor 4 Expression.

ABSTRACT: Cardiac hypertrophy is an adaptive response to various pathological insults, including hypertension. However, sustained hypertrophy can cause impaired calcium regulation, cardiac dysfunction, and remodeling, accompanied by cardiac fibrosis. Our previous study identified miR-25 as a regulator of SERCA2a, and found that the inhibition of miR-25 improved cardiac function and reduced fibrosis by restoring SERCA2a expression in a murine heart failure model. However, the precise mechanism underlying the reduction in fibrosis following miR-25 inhibition remains unclear. Therefore, we postulate that miR-25 may have additional targets that contribute to regulating cardiac fibrosis. Using in silico analysis, Krüppel-like factor 4 (KLF4) was identified as an additional target of miR-25. Further exper

SUBMITTER: Lee C 

PROVIDER: S-EPMC10418969 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature