The differential effects of cAMP mobilizing agents on TGF-β-induced extracellular matrix in human lung-derived fibroblasts: insights into therapeutic targets for lung fibrosis.

ABSTRACT:

Background

Injury-repair responses typically induce tissue or organ scarring. Generally, cAMP-mobilizing agents inhibit the activation of fibroblasts and deposition of extracellular matrix. Some but not all cAMP-mobilizing agents inhibit fibrosis. Evidence suggests that inhaled treprostinil, a prostacyclin (IP) analog, increases intracellular cAMP levels [cAMP]_I, and slows the decline in pulmonary function in patients with idiopathic pulmonary fibrosis (IPF). However, the molecular mechanisms by which cAMP-mobilizing agents, including treprostinil, alter the expression of matrix proteins in human lung fibroblasts (HLF) remain unclear. Unlike other G_αs -coupled receptors, we posit that the antifibrotic properties of treprostinil are driven by cAMP-mobilizing-de

SUBMITTER: Orfanos S 

PROVIDER: S-EPMC12645740 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature