Abstract

Diabetic kidney disease (DKD) is a prevalent complication of diabetes mellitus and a leading cause of endstage renal disease. Renal tubular damage plays a significant role in the progression of DKD. Recent research has unveiled the potential role of Salt-Inducible Kinase 2 (SIK2) in preventing both the progression of DKD and renal tubular damage. SIK2, a protein kinase involved in glucose metabolism, energy homeostasis, and inflammation, has shown protective effects on the kidneys. Activation of SIK2 has been found to suppress inflammation, reduce oxidative stress, promote renal tubular cell survival, and enhance glucose metabolism. Moreover, SIK2 activation helps maintain the integrity of the renal tubular epithelial barrier, preventing tubular damage. These findings provide valuable insights into the development of therapeutic interventions targeting SIK2 activation for the prevention of DKD and renal tubular damage, potentially improving the lives of individuals with diabetes and reducing the burden of this debilitating condition. Further research is warranted to fully elucidate the underlying mechanisms and translate these findings into clinical applications.