Adipose immune microenvironment: catalyst of age-related adipose tissue dysfunction
摘要
Aging has profound effects on whole-body homeostasis. With age, adipose tissue undergoes marked alterations in immune microenvironment and distribution as well as a loss of immune and metabolic capacities. Immune cells and adipokines constitute the immune microenvironment of adipose tissue. Chronic low-grade inflammation is one of the prominent features of aged adipose tissue. Age-related inflammation not only disrupts adipose tissue homeostasis but also interferes with its metabolic functions, promoting the development of age-related diseases. Here, we summarize the age-related alterations of adipose tissue, highlight the immune landscape, and discuss the mechanisms by which immune cells and adipokines affect age-related adipose tissue dysfunction. We also outline therapeutic strategies targeting adipose tissue inflammation, aiming to improve adipose tissue function and promote healthy aging.
Graphical AbstractGraphical abstract summarizing the contribution of the immune microenvironment to adipose tissue aging. The NLRP3 inflammasome responds to the accumulation of damage-associated molecular pattern molecules (DAMPs), driving adipose tissue dysfunction and expansion of the age-related immune cell population. Dysfunctional immune cells and pro-inflammatory populations secrete factors and interact to promote chronic inflammation and metabolic disorders. Meanwhile, aged adipose tissue exhibits altered adipokine secretion and disrupts immune and metabolic homeostasis. Created with BioRender.com.