Caspase-9 activates β-catenin signaling to promote pulmonary fibrosis.

ABSTRACT:

Background

Pulmonary fibrosis (PF) is a progressive interstitial lung disease marked by extracellular matrix accumulation and epithelial damage, with limited therapeutic options. Alveolar epithelial cell apoptosis is a key pathological hallmark of PF, but the upstream regulators driving this process remain unclear. Caspase-9, a central initiator of the intrinsic apoptotic pathway, has been implicated in fibrotic diseases across multiple organs. However, its role in lung fibrosis and its molecular interactions are not fully elucidated.

Methods

Caspase-9 expression was analyzed in human PF lung tissues, bleomycin (BLM)-induced mouse models, and TGF-β1-treated MLE-12 alveolar epithelial cells. Functional studies included pharmacological inhibition, siRNA knockdown, and overexpr

SUBMITTER: Wang J 

PROVIDER: S-EPMC12406446 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature