Podocyte specific deletion of PKM2 ameliorates LPS-induced podocyte injury through beta-catenin.

ABSTRACT:

Background

Acute kidney injury (AKI) is associated with a severe decline in kidney function caused by abnormalities within the podocytes' glomerular matrix. Recently, AKI has been linked to alterations in glycolysis and the activity of glycolytic enzymes, including pyruvate kinase M2 (PKM2). However, the contribution of this enzyme to AKI remains largely unexplored.

Methods

Cre-loxP technology was used to examine the effects of PKM2 specific deletion in podocytes on the activation status of key signaling pathways involved in the pathophysiology of AKI by lipopolysaccharides (LPS). In addition, we used lentiviral shRNA to generate murine podocytes deficient in PKM2 and investigated the molecular mechanisms mediating PKM2 actions in vitro.

Results

Specific PKM2 deletion

SUBMITTER: Alquraishi M 

PROVIDER: S-EPMC9150347 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature