{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gonzalez-Hurtado E"],"funding":["Aging Biology Foundation","NIDDK NIH HHS","NIA NIH HHS","NIAID NIH HHS","Foundation for the National Institutes of Health","Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)","American Federation for Aging Research","Cure Alzheimer&apos;s Fund","NIAMS NIH HHS"],"pagination":["1828-1843"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12443591"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5(9)"],"pubmed_abstract":["Age-related inflammation or 'inflammaging' increases disease burden and controls lifespan. Adipose tissue macrophages (ATMs) are critical regulators of inflammaging; however, the mechanisms involved are not well understood in part because the molecular identities of niche-specific ATMs are unknown. Using intravascular labeling to exclude circulating myeloid cells followed by single-cell sequencing with orthogonal validation via multiparametric flow cytometry, we define sex-specific changes and diverse populations of resident ATMs through lifespan in mice. Aging led to depletion of vessel-associated macrophages, expansion of lipid-associated macrophages and emergence of a unique subset of CD38<sup>+</sup> age-associated macrophages in visceral adipose tissue with inflammatory phenotype. Not"],"journal":["Nature aging"],"pubmed_title":["Nerve-associated macrophages control adipose homeostasis across lifespan and restrain age-related inflammation."],"pmcid":["PMC12443591"],"funding_grant_id":["AR070811","P01 AG051459","R01 AI143861","P01AG051459","R01 AI188824","R01 AR070811","R01 DK138675"],"pubmed_authors":["Shepard TM","Kluger Y","Damani-Yokota P","Goldberg EL","Gonzalez-Hurtado E","Li K","Qu R","Dixit VD","Gonzalez D","Sidorov S","Camell C","Khanna KM","Leveau C","Khairallah C","Mishra M","Artyomov MN","Yeung ST"],"additional_accession":[]},"is_claimable":false,"name":"Nerve-associated macrophages control adipose homeostasis across lifespan and restrain age-related inflammation.","description":"Age-related inflammation or 'inflammaging' increases disease burden and controls lifespan. Adipose tissue macrophages (ATMs) are critical regulators of inflammaging; however, the mechanisms involved are not well understood in part because the molecular identities of niche-specific ATMs are unknown. Using intravascular labeling to exclude circulating myeloid cells followed by single-cell sequencing with orthogonal validation via multiparametric flow cytometry, we define sex-specific changes and diverse populations of resident ATMs through lifespan in mice. Aging led to depletion of vessel-associated macrophages, expansion of lipid-associated macrophages and emergence of a unique subset of CD38<sup>+</sup> age-associated macrophages in visceral adipose tissue with inflammatory phenotype. Not","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-03T10:12:41.268Z","creation":"2026-04-26T03:11:42.848Z"},"accession":"S-EPMC12443591","cross_references":{"pubmed":["40897908"],"doi":["10.1038/s43587-025-00952-9"]}}