MiR-335-3p attenuates transforming growth factor beta 1-induced fibrosis by suppressing Thrombospondin 1.

ABSTRACT: Pulmonary fibrosis is characterized by excessive extracellular matrix (ECM) accumulation caused by detrimental stimuli. The progressive impairment in lung functions is chronic and highly fatal, presenting itself as a global health challenge. Because of the lack of efficacious treatments, the underlying mechanism should be investigated. The progression of fibrosis involves transforming growth factor-beta 1 (TGF-β1), which accelerates ECM production via epithelial-mesenchymal transition and cell invasion. As microRNAs (miRNAs) serve as regulators of disease development and progression, this study aimed to investigate the interaction of miRNAs and target genes that could contribute to pulmonary fibrosis when exposed to TGF-β1. Differentially expressed mRNA and miRNA were identified in respira

SUBMITTER: Han DH 

PROVIDER: S-EPMC11457990 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature