Obesity and type-2 diabetes as inducers of premature cellular senescence and ageing

Dominick G.A. Burton, Richard G.A. Faragher

    Research output: Contribution to journalArticlepeer-review


    Cellular senescence is now considered as a major mechanism in the development and progression of various diseases and this may include metabolic diseases such as obesity and type-2 diabetes. The presence of obesity and diabetes is a major risk factor in the development of additional health conditions, such as cardiovascular disease, kidney disease and cancer. Since senescent cells can drive disease development, obesity and diabetes can potentially create an environment that accelerates cell senescence within other tissues of the body. This can consequently manifest as age-related biological impairments and secondary diseases. Cell senescence in cell types linked with obesity and diabetes, namely adipocytes and pancreatic beta cells will be explored, followed by a discussion on the role of obesity and diabetes in accelerating ageing through induction of premature cell senescence mediated by high glucose levels and oxidised low-density lipoproteins. Particular emphasis will be placed on accelerated cell senescence in endothelial progenitor cells, endothelial cells and vascular smooth muscle cells with relation to cardiovascular disease and proximal tubular cells with relation to kidney disease. A summary of the potential strategies for therapeutically targeting senescent cells for improving health is also presented.

    Original languageEnglish
    Pages (from-to)447–459
    Issue number6
    Publication statusPublished - 27 Jul 2018


    • Ageing
    • Diabetes
    • Glucose
    • Obesity
    • ox-LDL
    • Senescence


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