Abstract
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 ABSTRACT: Graphical 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. [Image: see text]