The role of cellular senescence in diabetes mellitus and osteoporosis: molecular pathways and potential interventions.

Abstract

The improving effectiveness of health care leads inevitably to a rapid increase in the elderly population worldwide. At advanced ages, however, people experience chronic disabilities, which significantly increase the social and economic burden while curtailing survival, independence, and quality of life of the aging population. As aging is a multifactorial process, apart from genetic predisposition, other environmental factors, such as chronic sterile inflammation and cellular senescence, contribute as crucial participants and have been targeted to reverse their deleterious effects on tissue homeostasis and functional integrity. Cellular senescence refers to the essentially irreversible inhibition of cellular proliferation when cells are subjected to extrinsic or endogenous stress. Although the process of cellular senescence has long been known, recent evidence demonstrated that it characterizes many aging phenotypes and that elimination of senescent cells at the tissue level can improve age-related tissue dysfunction. These observations have renewed scientific interest in possible therapeutic interventions. Two major chronic diseases associated with aging that impose an enormous burden on global health systems are type 2 diabetes and osteoporosis. This review presents current data on (i) the underlying molecular mechanisms of cellular senescence, (ii) its relationship to these two endocrine diseases that are today prevalent worldwide, and (iii) future prospects of targeted intervention with the aim of simultaneously improving the progression and prognosis of these serious problems of aging.