Activin A Inhibitory Peptides Suppress Fibrotic Pathways by Targeting Epithelial-Mesenchymal Transition and Fibroblast-Myofibroblast Transformation in Idiopathic Pulmonary Fibrosis.

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a progressive and incurable chronic interstitial lung disease characterized by excessive fibrosis and impaired lung function. Current treatments, such as pirfenidone and nintedanib, slow disease progression but fail to halt or reverse fibrosis, highlighting the need for novel approaches. Activin A, which belongs to the TGF-β superfamily, is implicated in various fibrosis-related mechanisms, including epithelial-mesenchymal transition (EMT), a process where epithelial cells acquire mesenchymal characteristics, and fibroblast-myofibroblast transformation (FMT), in which fibroblasts differentiate into contractile myofibroblasts. It also promotes inflammatory cytokine release and extracellular matrix buildup. This study aimed to inhibit Activin A activity

SUBMITTER: Bastos VAF 

PROVIDER: S-EPMC11942258 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature