{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pan Y"],"funding":["Veterans Administration","NIDDK NIH HHS","NIH-NIDDK","National Natural Science Foundation of China","NIDDK"],"pagination":["e152391"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9057601"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["132(9)"],"pubmed_abstract":["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. Ther"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Cyclooxygenase-2 in adipose tissue macrophages limits adipose tissue dysfunction in obese mice."],"pmcid":["PMC9057601"],"funding_grant_id":["00507969","81870490","R01 DK054902","U24 DK059637","DK51265","DK059637","DK62794","DK054902","DK95785"],"pubmed_authors":["Pan Y","Fan X","Niu A","Wasserman DH","Jiang M","Arroyo JP","Terker AS","Tang J","Harris RC","Zhang MZ","Wang S","Zhang Y","Cao S","Wang Y"],"additional_accession":[]},"is_claimable":false,"name":"Cyclooxygenase-2 in adipose tissue macrophages limits adipose tissue dysfunction in obese mice.","description":"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. Ther","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2025-04-04T14:49:26.425Z","creation":"2025-04-04T14:49:26.425Z"},"accession":"S-EPMC9057601","cross_references":{"pubmed":["35499079"],"doi":["10.1172/JCI152391"]}}