Skeletal Senescence with Aging and Type 2 Diabetes

다국어 초록 (Multilingual Abstract)

Osteoporosis and type 2 diabetes (T2D) are common diseases that often coexist. While both of these diseases are associated withpoor bone quality and increased fracture risk, their pathogenesis of increased fracture risk differs and is multifactorial. Mounting evidence now indicates that key fundamental mechanisms that are central to both aging and energy metabolism exist. Importantly, thesemechanisms represent potentially modifiable therapeutic targets for interventions that could prevent or alleviate multiple complications of osteoporosis and T2D, including poor bone quality. One such mechanism that has gained increasing momentum is senescence, which is a cell fate that contributes to multiple chronic diseases. Accumulating evidence has established that numerous boneresident cell types become susceptible to cellular senescence with old age. Recent work also demonstrates that T2D causes the premature accumulation of senescent osteocytes during young adulthood, at least in mice, although it remains to be seen which otherbone-resident cell types become senescent with T2D. Given that therapeutically removing senescent cells can alleviate age-relatedbone loss and T2D-induced metabolic dysfunction, it will be important in future studies to rigorously test whether interventions thateliminate senescent cells can also alleviate skeletal dysfunction in context of T2D, as it does with aging.