Aging, Cellular Senescence and Diabetes Mellitus: Clinicopathological Correlates, Trends and Targets

Abstract

Diabetes and aging correlate with identical organ and system perturbations which are enhanced by concomitant molecular processes such as cellular senescence. Age represents a major risk factor for type 2 diabetes mellitus. It is unclear how senescence contributes to diabetes pathogenesis. Thus, available treatment modalities have not targeted the vital area of the disease. Reversal of untoward features of cellular aging represents a formidable trajectory for novel type 2 diabetes therapies where dissipation of pancreatic beta cells are impaired for insulin secretion. Furthermore, appropriate therapeutic modalities require characterization of defined senescent beta cell populations and the spatiotemporal variations of the expression of senescence genes. Aging is a dynamic public health dilemma in the prevailing demographic transitions in which a vast majority of those from the sixth decade of life increase exponentially in populations. Researchers have attempted to explicate senescence mechanisms via the identification of novel factors which interact with aging and age-related disorders in furtherance of treatment management, quality of life and lifespan regarding diabetes and its complications. An elucidation of the fundamental mechanisms which result in aging and research-oriented focus on healthy aging will mitigate numerous socioeconomic and healthcare encumbrance now and in the future for diabetes mellitus and related conditions.