Endothelial Autophagy Defect in NASH Patients Promotes Inflammation & Fibrosis

Commentary

Autophagy is a physiological process controlling endothelial homeostasis in vascular beds outside the liver. This original study demonstrates that autophagy is defective in liver endothelial cells of patients with NASH and that this defect promotes liver inflammation and fibrosis at early stages of NASH, but also at advanced stages of chronic liver disease. This study thus provides new insights into our understanding of the role of LSECs in the development of NASH and liver fibrosis. Targeting specifically liver endothelial autophagy may be an attractive strategy for NASH treatment.