ANRIL upregulates TGFBR1 to promote idiopathic pulmonary fibrosis in TGF-β1-treated lung fibroblasts via sequestering let-7d-5p.

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a progressive and life-threatening respiratory disease characterized by worsening lung function due to excessive scarring. The objective of this study was to investigate the role of the long non-coding RNA ANRIL (antisense non-coding RNA in the INK4 locus) in the development of IPF. Our research revealed a significant increase in ANRIL expression in pulmonary fibrosis, consistent with prior studies indicating elevated ANRIL levels in fibrotic tissues. In vitro experiments demonstrated that elevated ANRIL expression promoted fibroblast activation, as evidenced by the upregulation of fibrosis-related markers. Mechanistically, we found that ANRIL interacts with let-7d-5p, a microRNA involved in gene regulation, acting as a sponge for let-7d-5p. Fu

SUBMITTER: Wu W 

PROVIDER: S-EPMC11610569 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature