p53-miR-34a Feedback in Lung Fibroblasts Regulates Antifibrotic Effects of CSP7, Nintedanib and Pirfenidone.

Idiopathic pulmonary fibrosis (IPF) is a fatal disease characterized by progressive and irreversible loss of lung function. CSP7 exerts anti-fibrotic effects on fibrotic lung (myo)fibroblasts, which are the primary effector cells in progressive pulmonary fibrosis (PF) restoring p53-microRNA-34a-feedback induction. However, p53-microRNA-34a's role in the anti-fibrotic effects of Nintedanib and Pirfenidone have not been explored.

Exploring lichen-derived compounds as potential anti-cervical cancer agents: an DFT and MD simulation analysis.

Lichen-derived compounds have demonstrated promising anti-cancer potential, attributed to their bioavailability and unique structural properties. This study evaluates the therapeutic efficacy of five lichen compounds-fumarprotocetraric acid, salazinic acid, evernic acid, sekikaic acid, and lobaric acid-against cervical cancer, using molecular docking, density functional theory (DFT), and molecular dynamics (MD) simulations. Drug-likeness validation confirmed that evernic acid, topotecan, and ifosfamide adhere to Lipinski's rule of five.

Vascular protection by young circulating extracellular vesicles ameliorates aging-related pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a fatal, aging-related disease characterized by aberrant lung remodeling and progressive scarring, leading to organ failure and death. Current FDA-approved antifibrotic treatments are unable to reverse established disease, highlighting the need for innovative therapeutic approaches targeting novel pathways and cell types. Mounting evidence, including our own, has recently highlighted the pathogenic role of aging-related endothelial abnormalities, including vascular inflammation and oxidative stress, in the progression of lung fibrosis, offering new therapeutic opportunities to block IPF progression.