Autophagy activation contributes to lipid accumulation in tubular epithelial cells during kidney fibrosis.

ABSTRACT: Sustained activation of autophagy and lipid accumulation in tubular epithelial cells (TECs) are both associated with the kidney fibrosis progression. Autophagy has been found involved in the lipid metabolism regulation through a bi-directional mechanism of inducing lipolysis as well as promoting lipid droplet formation. However, whether and how autophagy influences lipid accumulation in kidney fibrosis remain unclear. In the current study, we show that UUO-induced lipid accumulation in tubular cells was significantly reduced when the pharmacological inhibitor 3-MA or CQ was administrated both in vivo and in vitro. Of interest, colocalization of LDs and autophagosomes, as well as colocalization of LDs and lysosomes were undetected in UUO-induced fibrotic kidneys, although lysosome function

SUBMITTER: Yan Q 

PROVIDER: S-EPMC6060103 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature