HSPA12A acts as a scaffolding protein to inhibit cardiac fibroblast activation and cardiac fibrosis.

ABSTRACT:

Introduction

Cardiac fibrosis is the main driver for adverse remodeling and progressive functional decline in nearly all types of heart disease including myocardial infarction (MI). The activation of cardiac fibroblasts (CF) into myofibroblasts is responsible for cardiac fibrosis. Unfortunately, no ideal approach for controlling CF activation currently exists.

Objectives

This study investigated the role of Heat shock protein A12A (HSPA12A), an atypical member of the HSP70 family, in CF activation and MI-induced cardiac fibrosis.

Methods

Primary CF and Hspa12a knockout mice were used in the experiments. CF activation was indicated by the upregulation of myofibroblast characters including alpha-Smooth muscle actin (αSMA), Collagen, and Fibronectin. Cardiac fibrosis was

SUBMITTER: Mao Q 

PROVIDER: S-EPMC11725103 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature