Trim38 attenuates pressure overload‑induced cardiac hypertrophy by suppressing the TAK1/JNK/P38 signaling pathway.

ABSTRACT: Pathological cardiac hypertrophy is a major contributor to heart failure (HF), resulting in high mortality rates worldwide; therefore, identifying key molecules in pathological cardiac hypertrophy is of critical importance for preventing or reversing HF. Tripartite motif 38 (Trim38) is an E3 ubiquitin ligase that serves a pivotal role in various diseases. The present study aimed to elucidate the regulatory role of Trim38 in pressure overload‑induced pathological cardiac hypertrophy and to explore its underlying molecular mechanisms. The expression of Trim38 was decreased in hypertrophic heart tissues from a murine model of transverse aortic constriction (TAC) and in neonatal rat cardiomyocytes (NRCMs) treated with phenylephrine (PE). Furthermore, Trim38 knockout (Trim38‑KO) aggravated card

SUBMITTER: Pang Y 

PROVIDER: S-EPMC12045468 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature