The Interaction of Diet and Cellular Senescence in Aging

The authors here tout a discussion of diet and cellular senescence, but in fact deliver a discussion on obesity, calorie restriction, and cellular senescence. One of the mechanisms by which excess visceral fat tissue causes chronic inflammation and pathology is by increasing the pace at which senescent cells are produced. The number of lingering senescent cells increases with age, and these cells disrupt the function of the immune system and surrounding tissue via their inflammatory secretions. Calorie restriction, on the other hand, upregulates stress response mechanisms that can slow the pace at which senescent cells are created. It also preserves the function of the immune system into later life, thereby increasing the pace at which they are destroyed by the immune system at any given age.

Normal human cells do not divide indefinitely. When cultured in vitro, cells can undergo only a finite number of divisions before entering in a nondividing state, the so-called replicative senescence. Senescence has been suggested both as contribute and a consequence of the ageing process and is involved in the development of many age-related chronic diseases. Cellular senescence is a state of an irreversible growth arrest that occurs in response to various forms of cellular stress and is characterized by a pro-inflammatory secretory phenotype.

Multiple studies showed that cellular senescence occurs in both physiological and pathophysiological conditions. Senescent cells accumulate with ageing and can contribute to age-related decline in tissue function. Obesity is a metabolic condition that can accelerate the ageing process by promoting a premature induction of the senescent state of the cells. In contrast, caloric restriction without malnutrition is currently the most effective non-genetic intervention to delay ageing, and its potential in decreasing the cellular senescent burden is suggested.

The precise mechanisms underlying the effect of obesity in the induction of premature cellular senescence are poorly understood and warrant further investigation. Moreover, more studies are required to understand how lowering calories intake reduces cellular senescence burden, and whether this can directly lower levels of molecules involved in the inflammation process, like interleukins, which, for instance, could also be promoted by other variables independently altered by senescence. Plus, in obesity and ageing studies, the researchers tend to focus on one specific organ or pathology type, which limits the information that may be collected about the temporal biological order of senescence induction. Thus, more in vitro studies are required especially in cellular model systems that can replicate the alterations seen during in vivo progression in the ageing process.



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