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Nutrient-Sensitive Senescence Checkpoints in Diabetic Kidney Disease
Rui Ji1, Qian Yang2, Hongtu Hu1,2
1Department of Nephrology, Chongqing Key Laboratory of Prevention and Treatment of Kidney Disease, Chongqing Clinical Research Center of Kidney and Urology Diseases, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
Article Highlights:
Diabetic kidney disease remains progressive in many patients despite modern cardiorenal therapies, suggesting that additional persistent cell fate pathways sustain kidney injury. An unresolved question is how nutrient-derived signals determine whether renal cells undergo adaptive repair or maladaptive senescence-like dysfunction. Amino acid flux, mitophagy, lipid routing, redox balance, endoplasmic reticulum proteostasis, and inflammatory danger signaling may form nutrient-sensitive senescence checkpoints in diabetic kidney disease. Distinguishing cell cycle arrest in proliferative cells from composite senescence-like injury in postmitotic cells may improve biomarker-based patient stratification and guide metabolism-informed senescence-targeted therapies.
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