Y. S. Prakash

This study investigates the role of Piezo1/2 channels in airway smooth muscle cells of COPD patients, finding altered expression and function linked to ECM changes.

This study identifies MPO as a post-translational inhibitor of CatK, linking acute inflammation to sustained fibrosis through impaired collagen degradation.

This study shows that MPST is essential for maintaining mitochondrial metabolic integrity in neonatal airway epithelial cells, and its loss under hyperoxia disrupts epithelial differentiation and contributes to airway injury.

This study shows that hyperoxia impairs mitochondrial function and epithelial differentiation in neonatal airway cells through proteomic analysis and metabolic reprogramming.

This study shows that loss of miR-153 promotes EndMT in lung endothelial cells, leading to vascular permeability and remodeling in pulmonary hypertension.

This study shows that TGF-β1-induced endothelial-to-mesenchymal transition in human lung vascular endothelial cells is Ca²⁺-dependent through store-operated Ca²⁺ entry via STIM1/Orai1 channels.

The paper identifies fibroblast-derived osteoglycin as a key factor promoting epithelial cell repair and presents its active fragment as a potential therapeutic for lung diseases.

This study shows that activating PIEZO1 reduces cyst formation in kidney cells and ex vivo models, suggesting it could be a therapeutic target for ADPKD.

This study identifies seven age-associated ECM proteins with increased expression in human lung tissue and demonstrates age-related differences in specific lung compartments.

This study shows TSLP enhances hypoxia-induced PA smooth muscle proliferation and contractility via Stat3 and PI3/Akt pathways, linking inflammation to pulmonary hypertension.