Integrin-Linked Kinase (ILK) Promotes Mitochondrial Dysfunction by Decreasing CPT1A Expression in a Folic Acid-Based Model of Kidney Disease.

ABSTRACT: Integrin-linked kinase (ILK) is a key scaffolding protein between extracellular matrix protein and the cytoskeleton and has been implicated previously in the pathogenesis of renal damage. However, its involvement in renal mitochondrial dysfunction remains to be elucidated. We studied the role of ILK and its downstream regulations in renal damage and mitochondria function both in vivo and vitro, using a folic acid (FA)-induced kidney disease model. Wild type (WT) and ILK conditional-knockdown (cKD-ILK) mice were injected with a single intraperitoneal dose of FA and studied after 15 days of chronic renal damage progression. Human Kidney tubular epithelial cells (HK2) were transfected with specific siRNAs targeting ILK, glycogen synthase kinase 3-β (GSK3β), or CCAAT/enhancer binding protein-β

SUBMITTER: de la Serna-Soto M 

PROVIDER: S-EPMC11899702 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature