Key result
Adipose tissue macrophages exhibit diverse phenotypes beyond the traditional M1/M2 classification, with obesity driving the accumulation of lipid-associated macrophages that regulate immunometabolism.
Why the study?
Recent understanding of adipose tissue macrophage diversity departs from the traditional M1 versus M2 paradigm, revealing a broader spectrum of phenotypes and functions in brown and white adipose tissue.
This review summarizes the evolving understanding of adipose tissue macrophage diversity and their critical roles in metabolic homeostasis and obesity-induced inflammation.
May inform obesity immunometabolic therapies; leaves open validation of diverse macrophage targeting in humans.
BACKGROUND: Adipose tissue macrophages (ATMs) are a well characterized regulator of adipose tissue inflammatory tone. Previously defined by the M1 vs M2 classification, we now have a better understanding of ATM diversity that departs from the old paradigm and reports a spectrum of ATM function and phenotypes in both brown and white adipose tissue. SCOPE OF REVIEW: This review provides an updated overview of ATM activation and function, ATM diversity in humans and rodents, and novel ATM functions that contribute to metabolic homeostasis and disease. MAJOR CONCLUSIONS: While the paradigm that resident ATMs predominate in the lean state and obesity leads to the accumulation of lipid-associated and inflammatory ATMs still broadly remains rigorously supported, the details of this model continue to be refined and single cell data provide new insight into ATM subtypes and states.
No takes yet. Share an insight, caveat, or question.
Nance et al. (2022) conducted a review in Obesity and adipose tissue inflammation. Adipose tissue macrophages exhibit diverse phenotypes beyond the traditional M1/M2 classification, with obesity driving the accumulation of lipid-associated macrophages that regulate immunometabolism.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: