Why the study?
Understanding mechanisms of adipose tissue dysfunction in obesity can provide deeper insight into processes contributing to aging-related metabolic dysfunction.
Key points are not available for this paper at this time.
Design
Review
Obesity may accelerate aging-like cardiovascular risk; leaves open whether targeting shared pathways alters outcomes.
Obesity is associated with an increased risk of acute and chronic diseases, including hypertension, stroke, myocardial infarction, cardiovascular pathologies, diabetes, and cancer; it also reduces life expectancy by up to 20 years, increasing the risk of premature death. It has been shown that obesity-associated metabolic changes are similar to those observed in aging. For example, obesity and aging share a similar range of phenotypes, such as genome disintegration, mitochondrial dysfunction, accumulation of intracellular macromolecules, weakened immune system, and systemic inflammation. The commonality of mechanisms may underlie the acceleration of aging processes, both at molecular and systemic levels. Thus, the understanding of the mechanisms of adipose tissue dysfunction in obesity can provide deeper insight into the processes that contribute to aging-related metabolic dysfunction. The present review addresses the molecular and cellular mechanisms that underlie obesity and aging, as well as the issue of how obesity can activate aging, initiating the early onset of aging-related chronic diseases.
No takes yet. Share an insight, caveat, or question.
Dyleva et al. (2023) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: