Mechanism of Mitochondrial Dysfunction By Inhaled Toxicants
Cigarette smoke (CS), the most important etiological risk factor for the development of COPD/emphysema, causes lung injurious and damaging responses. These effects include mitochondrial dysfunction and defective mitophagy (removal of damaged mitochondria from a cell prior to cell death). We are studying CS-induced mitochondrial dysfunction leads to defective mitophagy by disrupting the protective shelterin telomere capping protein complex, and that healthy mitochondrial transfer into damaged lung epithelial cells protects against CS-induced injurious responses in COPD/emphysema. The outcome will provide information on attenuation of the telomere shelterin complex and fresh mitochondria transfer can be utilized as novel therapeutic targets for the treatment/management of COPD/emphysema.
