Suppression of SMOC2 alleviates myocardial fibrosis via the ILK/p38 pathway.

ABSTRACT:

Background

Fibrosis of the myocardium is one of the main pathological changes of adverse cardiac remodeling, which is associated with unsatisfactory outcomes in patients with heart disease. Further investigations into the precise molecular mechanisms of cardiac fibrosis are urgently required to seek alternative therapeutic strategies for individuals suffering from heart failure. SMOC2 has been shown to be essential to exert key pathophysiological roles in various physiological processes in vivo, possibly contributing to the pathogenesis of fibrosis. A study investigating the relationship between SMOC2 and myocardial fibrosis has yet to be conducted.

Methods

Mice received a continuous ISO injection subcutaneously to induce cardiac fibrosis, and down-regulation of SMOC2

SUBMITTER: Rui H 

PROVIDER: S-EPMC10017443 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature