Takeo Ishikawa

TL;DR: It is demonstrated that CSE transiently induces activation of autophagy in HBEC, followed by accelerated cell senescence and concomitant accumulation of p62 and ubiquitinated proteins, suggesting a novel protective role for autophagic clearance of damaged proteins in the tobacco smoke-inducedsenescence-associated lung disease, COPD.

TL;DR: In vitro experiments showed PRKN overexpression was sufficient to induce mitophagy during CSE exposure even in the setting of reduced PINK1 protein levels, resulting in attenuation of mitochondrial ROS production and cellular senescence.

TL;DR: It is found that PFD induced autophagy/mitophagy activation via enhanced PARK2 expression, which was partly involved in the inhibition of myofibroblast differentiation in the presence of TGF-β, which may at least partly explain the anti-fibrotic mechanisms of PFD for IPF treatment.

TL;DR: The results suggest that AZM suppresses NOX4 by promoting proteasomal degradation, resulting in inhibition of TGFB-induced myofibroblast differentiation and lung fibrosis development.

TL;DR: The role of CKB is investigated in cigarette smoke extract (CSE)-induced cellular senescence in human bronchial epithelial cells (HBECs) and expression levels were reduced in HBECs from patients with COPD compared with that of HB ECs from nonsmokers.