Tubular Mas receptor mediates lipid-induced kidney injury.

ABSTRACT: Obesity-related kidney diseases are becoming serious health problems worldwide, yet the mechanism by which obesity causes kidney injury is not fully understood. The purpose of current study was to investigate the role of Mas receptor in lipid-induced kidney injury. In mice fed with high-fat diet (HFD), the protein abundance of markers of autophagy, endoplasmic reticulum stress (ER stress) and apoptosis was dramatically increased in the kidney cortex, which was markedly prevented by Mas deletion (Mas^-/-) or Mas receptor antagonist A779. Palmitic acid (PA) induced persistently increased autophagy, ER stress, and apoptosis as well as mitochondrial injuries in primary cultured proximal tubular cells from wild type, but not from Mas^-/- mice. In human proximal tubular HK2 c

SUBMITTER: Kong Y 

PROVIDER: S-EPMC7817966 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature