Role of STK38L in atrial fibrillation-associated myocardial fibrosis: findings from RNA-seq analysis.

ABSTRACT:

Background

Myocardial fibrosis is a key pathological feature of many cardiovascular diseases, leading to cardiac dysfunction. Transforming growth factor β1 (TGF-β1) induces the proliferation and activation of cardiac fibroblasts (CFs), key contributors to myocardial fibrosis. To explore the mechanism underlying myocardial fibrosis, we aimed to determine whether serine/threonine kinase 38 like (STK38L) contributes to the development of myocardial fibrosis by regulating the proliferation and activation of CFs triggered by TGF-β1.

Methods

In this study, atrial tissue samples from atrial fibrillation (AF) patients with features of myocardial fibrosis (a category of atrial cardiomyopathy) and sinus rhythm (SR) patients without myocardial fibrosis were collected for RNA sequencing

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC11538834 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature