Mitochondrial Fission Mediated Cigarette Smoke-induced Pulmonary Endothelial Injury.

ABSTRACT: Cigarette smoke (CS) exposure increases the risk for acute respiratory distress syndrome in humans and promotes alveolar-capillary barrier permeability and acute lung injury in animal models. However, the underlying mechanisms are not well understood. Mitochondrial fusion and fission are essential for mitochondrial homeostasis in health and disease. In this study, we hypothesized that CS caused endothelial injury via an imbalance of mitochondrial fusion and fission and resultant mitochondrial oxidative stress and dysfunction. We noted that CS altered mitochondrial morphology by shortening mitochondrial networks and causing perinuclear accumulation of damaged mitochondria in primary rat lung microvascular endothelial cells. We also found that CS increased mitochondrial fission likely by dec

SUBMITTER: Wang Z 

PROVIDER: S-EPMC7605166 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature