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Journal of Diabetes & Clinical Practice
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  • Review Article   
  • J Diabetes Clin Prac 2023, Vol 6(3): 185
  • DOI: 10.4172/jdce.1000185

The Progression of Diabetic Kidney Disease and Renal Tubular Damage are Both Prevented by SIK2

Dr. Jhrna M*
Department of Diabetology, University of California, USA
*Corresponding Author : Dr. Jhrna M, Department of Diabetology, University of California, USA, Email: mjhrna8658@gmail.com

Received Date: Apr 10, 2023 / Accepted Date: May 03, 2023 / Published Date: May 08, 2023

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.

Citation: Jhrna M (2023) The Progression of Diabetic Kidney Disease and Renal Tubular Damage are Both Prevented by SIK2. J Diabetes Clin Prac 6: 185. Doi: 10.4172/jdce.1000185

Copyright: © 2023 Jhrna M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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