Inhibited adipogenesis and low-grade inflammation enhance adipocyte hypertrophy in aging adipose tissue

Abstract Adipose tissue mass grows through an increase in the number (adipogenesis) and size (lipogenesis) of adipocytes, and these processes change with age. Visceral adiposity and increased inflammation often accompany aging. Here, we review the factors and changes that influence adipogenesis, lipogenesis, and the inflammatory microenvironment of adipose tissue during aging with a focus on adipose stem cells and immune cells. Aging-associated cellular senescence and stem cell exhaustion inhibit adipocyte renewal, leading to excessive hypertrophy and low-grade inflammation. Moreover, the different adipose stem cell types can stimulate or inhibit adipogenesis. The removal rate of triglycerides stored in adipocytes decreases with age, but the results of studies regarding changes in the related enzymes and the effects on lifespan are conflicting. Adipogenesis inhibition induced by changes in the types and proportions of cells may be the primary driving force for adipose tissue aging and thus may be a target for anti-aging therapy. Due to the similarities between obesity and aging adipose tissue, studies have previously verified the roles of adipose stem cells, senescent cells, and immune cells in obesity, whereas studies in aged adipose tissue are sparse. Future studies should address the effects of changes in adipose stem cell subtypes and immune cells on the aging of adipose tissue, which may help to develop anti-aging therapies.