Adiponectin deficiency induces mitochondrial dysfunction and promotes endothelial activation and pulmonary vascular injury.

ABSTRACT: Adiponectin (APN), an adipocyte-derived adipokine, has been shown to limit lung injury originating from endothelial cell (EC) damage. Previously we reported that obese mice with low circulatory APN levels exhibited pulmonary vascular endothelial dysfunction. This study was designed to investigate the cellular and molecular mechanisms underlying the pulmonary endothelium-dependent protective effects of APN. Our results demonstrated that in APN^-/- mice, there was an inherent state of endothelium mitochondrial dysfunction that could contribute to endothelial activation and increased susceptibility to LPS-induced acute lung injury (ALI). We noted that APN^-/- mice showed decreased expression of mitochondrial biogenesis regulatory protein peroxisome proliferator-activated r

SUBMITTER: Shah D 

PROVIDER: S-EPMC6894062 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature