Impaired endothelial autophagy promotes liver fibrosis by aggravating the oxidative stress response during acute liver injury.

ABSTRACT:

Background & aims

Endothelial dysfunction plays an essential role in liver injury, yet the phenotypic regulation of liver sinusoidal endothelial cells (LSECs) remains unknown. Autophagy is an endogenous protective system whose loss could undermine LSEC integrity and phenotype. The aim of our study was to investigate the role of autophagy in the regulation of endothelial dysfunction and the impact of its manipulation during liver injury.

Methods

We analyzed primary isolated LSECs from Atg7^control and Atg7^endo mice as well as rats after CCl₄ induced liver injury. Liver tissue and primary isolated stellate cells were used to analyze liver fibrosis. Autophagy flux, microvascular function, nitric oxide bioavailability, cellular superoxide content

SUBMITTER: Ruart M 

PROVIDER: S-EPMC6704477 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature