Tubular mitochondrial pyruvate carrier disruption elicits redox adaptations that protect from acute kidney injury.

ABSTRACT:

Objective

Energy-intensive kidney reabsorption processes essential for normal whole-body function are maintained by tubular epithelial cell metabolism. Although tubular metabolism changes markedly following acute kidney injury (AKI), it remains unclear which metabolic alterations are beneficial or detrimental. By analyzing large-scale, publicly available datasets, we observed that AKI consistently leads to downregulation of the mitochondrial pyruvate carrier (MPC). This investigation aimed to understand the contribution of the tubular MPC to kidney function, metabolism, and acute injury severity.

Methods

We generated tubular epithelial cell-specific Mpc1 knockout (MPC TubKO) mice and employed renal function tests, in vivo renal ¹³C-glucose tracing, mechanistic enz

SUBMITTER: Rauckhorst AJ 

PROVIDER: S-EPMC10733108 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature