Podocyte aging and diabetic kidney disease

Kidney Int. 2025 Apr;107(4):596-598. doi: 10.1016/j.kint.2025.01.011.

Abstract

Podocyte injury causes a series of cellular changes, including hypertrophy, dedifferentiation, senescence, apoptosis, and detachment. Although evidence suggests a pivotal role of podocyte senescence in diabetic kidney disease, the exact triggers and underlying mechanism remain elusive. In this study, Li et al. uncover that GPR124, a G-protein-coupled receptor, protects against podocyte senescence by inhibiting focal adhesion kinase. These findings underscore that the GPR124/focal adhesion kinase axis could be a novel target for diabetic kidney disease therapy.

MeSH terms

  • Animals
  • Cellular Senescence*
  • Diabetic Nephropathies* / metabolism
  • Diabetic Nephropathies* / pathology
  • Focal Adhesion Protein-Tyrosine Kinases / antagonists & inhibitors
  • Focal Adhesion Protein-Tyrosine Kinases / metabolism
  • Humans
  • Podocytes* / drug effects
  • Podocytes* / metabolism
  • Podocytes* / pathology
  • Receptors, G-Protein-Coupled* / metabolism
  • Signal Transduction

Substances

  • Receptors, G-Protein-Coupled
  • Focal Adhesion Protein-Tyrosine Kinases