Baricitinib represses the myocardial fibrosis via blocking JAK/STAT and TGF-β1 pathways in vivo and in vitro.

ABSTRACT:

Background

JAK/STAT pathway is closely involved in the organ fibrotic process. The current study aimed to investigate the impact of baricitinib, an oral selective JAK1/JAK2 inhibitor, on the myocardial fibrosis in vivo and the activation of cardiac fibroblasts in vitro.

Methods

The mouse myocardial fibrosis model was established by isoproterenol (ISO) treatment, then was treated by baricitinib. The activation of mouse cardiac fibroblasts was established by TGF-β1 stimulation, then was treated by baricitinib with several concentrations. Besides, JAK2 was knocked down by small interfering RNA (siRNA) in TGF-β1-stimulated mouse cardiac fibroblasts.

Results

Baricitinib not only attenuated myocardial cell widening, inflammatory infiltration, fibrous tissue, and heart index

SUBMITTER: Feng R 

PROVIDER: S-EPMC11783835 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature