Related Experiment Video
Updated: Jan 10, 2026

08:15
Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
Published on: May 10, 2024
897
Harnessing ROCK biology to revolutionize diabetic nephropathy: decoding mechanisms, designing therapies
1Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, 3-25-8, Nishishimbashi, Minato-ku, Tokyo, 105-8461 Japan.
Diabetology International
|November 28, 2025
Summary
Small GTPases, specifically Rho-associated coiled-coil-containing protein kinase (ROCK) isoforms ROCK1 and ROCK2, are key drivers of diabetic kidney disease. Targeting ROCK signaling offers a promising therapeutic strategy for halting chronic kidney disease progression in diabetic patients.
Area of Science:
- Nephrology
- Molecular Biology
- Pharmacology
Background:
- Diabetic nephropathy is a leading cause of kidney failure worldwide.
- Current therapies leave residual risks, highlighting the need for novel treatment strategies.
- Small GTPases, particularly Rho-associated coiled-coil-containing protein kinase (ROCK) signaling, are implicated in diabetic kidney disease progression.
Purpose of the Study:
- To review the distinct pathophysiological roles of ROCK1 and ROCK2 isoforms in diabetic nephropathy.
- To explore the molecular mechanisms by which ROCK signaling contributes to kidney damage.
- To discuss the therapeutic potential of ROCK inhibitors for diabetic kidney disease and related disorders.
Main Methods:
- Comprehensive literature review of genetic and pharmacological studies.
- Analysis of ROCK isoform-specific functions in key pathological pathways.
- Integration of molecular insights with clinical implications for chronic kidney disease (CKD) management.
Main Results:
- ROCK1 regulates AMP-activated protein kinase-mediated fatty acid metabolism and mitochondrial dynamics.
- ROCK2 modulates peroxisome proliferator-activated receptor α signaling and inflammatory responses.
- ROCK signaling contributes to podocyte injury, glomerulosclerosis, tubular dysfunction, and metabolic disturbances.
Conclusions:
- ROCK1 and ROCK2 play distinct, critical roles in the pathogenesis of diabetic nephropathy.
- Targeting ROCK signaling, via ROCK inhibitors, presents a viable therapeutic avenue for diabetic kidney disease.
- Further research into isoform-specific inhibition could lead to more effective treatments for CKD in diabetic patients.

