biostudies-literaturePan YVeterans AdministrationNIDDK NIH HHSNIH-NIDDKNational Natural Science Foundation of ChinaNIDDKe152391https://www.ebi.ac.uk/biostudies/studies/S-EPMC9057601biostudies-literatureUnknown132(9)Obesity-associated complications are causing increasing morbidity and mortality worldwide. Expansion of adipose tissue in obesity leads to a state of low-grade chronic inflammation and dysregulated metabolism, resulting in insulin resistance and metabolic syndrome. Adipose tissue macrophages (ATMs) accumulate in obesity and are a source of proinflammatory cytokines that further aggravate adipocyte dysfunction. Macrophages are rich sources of cyclooxygenase (COX), the rate limiting enzyme for prostaglandin E2 (PGE2) production. When mice were fed a high-fat diet (HFD), ATMs increased expression of COX-2. Selective myeloid cell COX-2 deletion resulted in increased monocyte recruitment and proliferation of ATMs, leading to increased proinflammatory ATMs with decreased phagocytic ability. TherThe Journal of clinical investigationCyclooxygenase-2 in adipose tissue macrophages limits adipose tissue dysfunction in obese mice.PMC90576010050796981870490R01 DK054902U24 DK059637DK51265DK059637DK62794DK054902DK95785Pan YFan XNiu AWasserman DHJiang MArroyo JPTerker ASTang JHarris RCZhang MZWang SZhang YCao SWang YfalseCyclooxygenase-2 in adipose tissue macrophages limits adipose tissue dysfunction in obese mice.Obesity-associated complications are causing increasing morbidity and mortality worldwide. Expansion of adipose tissue in obesity leads to a state of low-grade chronic inflammation and dysregulated metabolism, resulting in insulin resistance and metabolic syndrome. Adipose tissue macrophages (ATMs) accumulate in obesity and are a source of proinflammatory cytokines that further aggravate adipocyte dysfunction. Macrophages are rich sources of cyclooxygenase (COX), the rate limiting enzyme for prostaglandin E2 (PGE2) production. When mice were fed a high-fat diet (HFD), ATMs increased expression of COX-2. Selective myeloid cell COX-2 deletion resulted in increased monocyte recruitment and proliferation of ATMs, leading to increased proinflammatory ATMs with decreased phagocytic ability. Ther2022-01-01T00:00:00Z2022 May2025-04-04T14:49:26.425Z2025-04-04T14:49:26.425ZS-EPMC90576013549907910.1172/JCI152391