FIGURE 10.

Working hypothesis depicts the critical role of AcSDKP in the kidney metabolism. Suppressed level of AcSDKP in diabetes is linked with SIRT3‐deficiency associated disruption in central metabolism and hence, fibrosis in kidney. POP inhibitor (S17092), partially blocks the AcSDKP level and hence further enhanced the severity of defective metabolism‐associated kidney fibrosis. ACE inhibition elevates the AcSDKP level, improve the renal metabolic health whereas, ARB does not alter the AcSDKP level , and hence, unable to improve the renal metabolic health in diabetic kidney, suggests that AcSDKP is essential peptide for renal metabolic health and protects from fibrosis