Copyright © 2026 Authors retain the copyright of this article. This article is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

@article{210879,
        author = {Suhas N Gowda and Nischitha H.S. and Swetha Jeevan and Ashmitha A. S},
        title = {Accelerated Ageing in type 2 diabetes mellitus: From Hyperglycaemia to Cellular Senescence},
        journal = {International Journal of Innovative Research in Technology},
        year = {2026},
        volume = {13},
        number = {6},
        pages = {2492-2505},
        issn = {2349-6002},
        url = {https://ijirt.org/article?manuscript=210879},
        abstract = {Type 2 diabetes mellitus (T2DM) is increasingly being studied in relation to the biological changes that occur during ageing. Persistent elevation of blood glucose may accelerate several cellular disturbances, including the accumulation of advanced glycation end products, excessive oxidative stress, mitochondrial impairment, DNA damage, and prolonged inflammatory activity. These changes may interact with key features of biological ageing, such as cellular senescence, telomere shortening, epigenetic alterations, disrupted autophagy, and declining stem-cell function. This narrative review explores how chronic hyperglycaemia may influence cellular senescence and examines the potential consequences of these interconnected mechanisms across different organs. It also discusses emerging biomarkers used to investigate biological ageing and reviews current diabetes treatments alongside potential interventions targeting age-related cellular dysfunction. Although established therapies play an important role in glycaemic control and reducing diabetes-associated complications, their ability to directly reverse or slow biological ageing remains incompletely understood. Similarly, senolytic agents and other geroscience-based interventions offer promising research directions but have not yet been established as routine treatments for T2DM. A clearer understanding of these mechanisms may help identify future therapeutic opportunities. However, well-designed longitudinal studies and clinical trials are required to determine whether targeting cellular senescence can meaningfully improve long-term health outcomes in people with T2DM.},
        keywords = {Type 2 Diabetes Mellitus; Cellular Senescence; Biological Ageing; Hyperglycaemia; Advanced Glycation End Products; Oxidative Stress; Inflammaging; Senolytics; Epigenetic Clocks; Telomere Shortening.},
        month = {November},
        }