Sirtuin 5 Regulates Proximal Tubule Fatty Acid Oxidation to Protect against AKI.

ABSTRACT:

Background

The primary site of damage during AKI, proximal tubular epithelial cells, are highly metabolically active, relying on fatty acids to meet their energy demands. These cells are rich in mitochondria and peroxisomes, the two organelles that mediate fatty acid oxidation. Emerging evidence shows that both fatty acid pathways are regulated by reversible posttranslational modifications, particularly by lysine acylation. Sirtuin 5 (Sirt5), which localizes to both mitochondria and peroxisomes, reverses post-translational lysine acylation on several enzymes involved in fatty acid oxidation. However, the role of the Sirt5 in regulating kidney energy metabolism has yet to be determined.

Methods

We subjected male Sirt5-deficient mice (either +/- or -/-) and wild-type controls,

SUBMITTER: Chiba T 

PROVIDER: S-EPMC6900790 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature