Cigarette smoke extract (CSE)-mediated  mitochondrial dysfunction, oxidative stress, cell apoptosis and inflammation can be reduced by the overexpression of prohibitin, reveals a recent study. The study, conducted by a team of researchers from the Institute of Respiratory Disease, Central South University, Changsha, Hunan, found that prohibitin expression was downregulated significantly in the lung tissues of the emphysema mouse model. Prohibitin protected hPMECs from CSE-induced apoptosis, inflammation, oxidative stress and mitochondrial dysfunction, highlighting the contribution of prohibitin to the maintenance of EC homeostasis under CSE, the study suggested. 

In addition, the team wrote that the effects are brought about by the reduction of inhibition of nuclear factor-kappa B (NF-κB) p65 accumulation and IκBα degradation induced by CSE.