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Traditionally, hyperglycemia has been regarded as a uniform stressor inducing cellular senescence; however, significant heterogeneity exists in different renal cell types\u2019 responses to high glucose (HG) stimulation. This review systematically elucidates mechanisms underlying senescence of major renal cell types under hyperglycemic conditions. Hyperglycemia acts as a common initiator triggering senescence via shared pathways, including oxidative stress and metabolic dysregulation. However, owing to distinct structural, functional, and molecular profiles across cell types, divergent senescence programs are activated. Specifically, podocyte senescence centers on GSK3\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2010mediated collapse of metabolic homeostasis and GPR124 axis\u2010related mechanosensing dysfunction; mesangial cell (MC) senescence manifests as STAT5\u2010 and Caveolin\u20101 signaling\u2010mediated \u201csenescence\u2013fibrosis\u201d vicious cycles; glomerular endothelial cell (GEC) senescence is characterized by dysregulation of the NOS\/NO signaling axis and glycocalyx damage; and renal tubular epithelial cell (TEC) senescence is initiated by mitochondrial damage under metabolic overload, promoting interstitial fibrosis through the senescence\u2010associated secretory phenotype (SASP). By revealing this heterogeneous mechanism shifting from \u201ccommon stress\u201d to \u201cspecific responses,\u201d this review offers a novel perspective on DKD pathogenesis and establishes a theoretical foundation for developing targeted anti\u2010senescence therapies. It further discusses implications for the clinical translation of renal protective agents.\n                  <\/jats:p>","DOI":"10.1155\/jdr\/9157351","type":"journal-article","created":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T09:57:21Z","timestamp":1777543041000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["From a Shared Stress to Cell\u2010Type\u2010Specific Responses: The Heterogeneous Mechanisms of High Glucose\u2010Induced Cellular Senescence in Diabetic Kidney 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