Anoctamin-1 is induced by TGF-beta and contributes to lung myofibroblast differentiation.
Eleanor B ReedShaina OrbetaAlbert SitikovIrena LevitanGökhan M MutluAlexander A MonginNickolai O DulinPublished in: bioRxiv : the preprint server for biology (2023)
Pulmonary fibrosis is a devastating disease characterized by progressive scarring of the lungs and resulting in deterioration of lung function. Myofibroblasts are cells produced from tissue fibroblasts during this disease and are the key pathologic cells that contribute to lung scaring. Transforming growth factor-beta (TGF-beta) is the cytokine that drives myofibroblast differentiation. This study identifies a novel role of a chloride channel, Anoctamin-1, in the cellular mechanism TGF-beta-induced myofibroblast differentiation.
Keyphrases
- transforming growth factor
- epithelial mesenchymal transition
- lung function
- induced apoptosis
- pulmonary fibrosis
- cell cycle arrest
- cystic fibrosis
- chronic obstructive pulmonary disease
- signaling pathway
- multiple sclerosis
- endoplasmic reticulum stress
- air pollution
- genome wide
- oxidative stress
- radiation therapy
- neoadjuvant chemotherapy
- dna methylation