Accelerated Kidney Aging in Diabetes Mellitus

Overview

Journal Oxid Med Cell Longev

Publisher Wiley

Specialties Cell Biology
Endocrinology

Date 2020 Aug 11

PMID 32774664

Citations 43

Authors

Jing Guo

Hui Juan Zheng

Wenting Zhang

Wenjiao Lou

Chenhui Xia

Xue Ting Han

Wei Jun Huang

Fan Zhang

Yaoxian Wang

Wei Jing Liu

Affiliations

Soon will be listed here.

Abstract

With aging, the kidney undergoes inexorable and progressive changes in structural and functional performance. These aging-related alterations are more obvious and serious in diabetes mellitus (DM). Renal accelerated aging under DM conditions is associated with multiple stresses such as accumulation of advanced glycation end products (AGEs), hypertension, oxidative stress, and inflammation. The main hallmarks of cellular senescence in diabetic kidneys include cyclin-dependent kinase inhibitors, telomere shortening, and diabetic nephropathy-associated secretory phenotype. Lysosome-dependent autophagy and antiaging proteins Klotho and Sirt1 play a fundamental role in the accelerated aging of kidneys in DM, among which the autophagy-lysosome system is the convergent mechanism of the multiple antiaging pathways involved in renal aging under DM conditions. Metformin and the inhibitor of sodium-glucose cotransporter 2 are recommended due to their antiaging effects independent of antihyperglycemia, besides angiotensin-converting enzyme inhibitors/angiotensin receptor blockers. Additionally, diet intervention including low protein and low AGEs with antioxidants are suggested for patients with diabetic nephropathy (DN). However, their long-term benefits still need further study. Exploring the interactive relationships among antiaging protein Klotho, Sirt1, and autophagy-lysosome system may provide insight into better satisfying the urgent medical needs of elderly patients with aging-related DN.

Citing Articles

Prevalence of and Factors Associated With Incidental Chronic Kidney Disease in Patients Newly Diagnosed With Type 2 Diabetes Mellitus.

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High glucose induces renal tubular epithelial cell senescence by inhibiting autophagic flux.

Zhang Y, Zhao Y, Liu Y, Fang Y, Sun L, Wei S Hum Cell. 2025; 38(2):43.

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Cellular Senescence: A Bridge Between Diabetes and Microangiopathy.

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Predictive value of bone metabolism markers in the progression of diabetic kidney disease: a cross-sectional study.

Kang Y, Jin Q, Zhou M, Li Z, Zheng H, Li D Front Endocrinol (Lausanne). 2024; 15:1489676.

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Oxidative stress and senescence in aging kidneys: the protective role of SIRT1.

Almalki W, Salman Almujri S EXCLI J. 2024; 23:1030-1067.

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