LMK235 ameliorates inflammation and fibrosis after myocardial infarction by inhibiting LSD1-related pathway.

ABSTRACT:

Background

Histone deacetylase 4 (HDAC4) and histone deacetylase 5 (HDAC5) are two isoforms of class IIa HDACs, and LMK235 is an HDAC inhibitor with higher selectivity for HDAC4/5. This study aimed to explore the expression and subcellular localization of HDAC4/5 and determine the mechanisms underlying the impact of LMK235 on ventricular remodelling post-MI.

Methods

The MI model was established by left anterior descending branch (LAD) ligation, and LMK235 or vehicle was intraperitoneally injected daily for 21 days. Cardiac function was determined by echocardiography. Inflammation was evaluated by HE staining and measuring inflammatory cytokine expression, and fibrosis was evaluated by Masson staining and measuring fibrotic biomarker expression.

Results

We found that L

SUBMITTER: Lv F 

PROVIDER: S-EPMC11461967 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature