{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T20:22:25Z","timestamp":1790626945945,"version":"4.1.0"},"reference-count":58,"publisher":"National Academy of Sciences","issue":"11","license":[{"start":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T00:00:00Z","timestamp":1741651200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000069","name":"HHS | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"publisher","award":["1R01AR074428"],"award-info":[{"award-number":["1R01AR074428"]}],"id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2025,3,18]]},"abstract":"\n Infiltrating macrophages contribute to muscle dystrophic changes in Duchenne muscular dystrophy (DMD). In a DMD mouse model,\n \n mdx\n 5cv<\/jats:sup>\n <\/jats:italic>\n mice, CC chemokine receptor type 2 (CCR2) deficiency diminishes Ly6C\n hi<\/jats:sup>\n macrophage infiltration by blocking blood Ly6C\n hi<\/jats:sup>\n inflammatory monocyte recruitment. This is accompanied by transient improvement of muscle damage, fibrosis, and regeneration. The benefit, however, is lost after the expansion of intramuscular Ly6C\n lo<\/jats:sup>\n macrophages. To address the mechanisms underlying the Ly6C\n lo<\/jats:sup>\n macrophage expansion, we compared\n \n mdx\n 5cv<\/jats:sup>\n \/Nur77\n \u2212\/\u2212<\/jats:sup>\n <\/jats:italic>\n and\n \n mdx\n 5cv<\/jats:sup>\n \/Ccr2\n \u2212\/\u2212<\/jats:sup>\n \/Nur7\n \u2212\/\u2212<\/jats:sup>\n <\/jats:italic>\n mice with\n \n mdx\n 5cv<\/jats:sup>\n <\/jats:italic>\n and\n \n mdx\n 5cv<\/jats:sup>\n \/Ccr2\n \u2212\/\u2212<\/jats:sup>\n <\/jats:italic>\n mice, respectively, and found no evidence to suggest Ly6C\n lo<\/jats:sup>\n monocyte recruitment by dystrophic muscles. Single-cell RNA sequencing analysis and\n \n Flt3\n cre<\/jats:sup>\n \/Rosa26\n LSL-YFP<\/jats:sup>\n <\/jats:italic>\n -based lineage tracing of macrophage origins demonstrated the expansion and pathogenic activation of muscle resident macrophages in CCR2-deficient\n \n mdx\n 5cv<\/jats:sup>\n <\/jats:italic>\n mice. The expansion was associated with increased cell proliferation, which appeared induced by colony-stimulating factor-1 (CSF-1) derived from fibro\/adipogenic progenitors (FAPs). Our study establishes a pathogenic role for skeletal muscle resident macrophages and supports a regulatory role of FAPs in stimulating the expansion of resident macrophages in the DMD mouse model when the inflammatory macrophage infiltration is inhibited.\n <\/jats:p>","DOI":"10.1073\/pnas.2410095122","type":"journal-article","created":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T13:48:46Z","timestamp":1741700926000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":11,"title":["Expansion and pathogenic activation of skeletal muscle\u2013resident macrophages in\n \n mdx\n 5cv<\/sup>\n \/Ccr2\n \u2212\/\u2212<\/sup>\n <\/i>\n mice"],"prefix":"10.1073","volume":"122","author":[{"given":"Yinhang","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Neurology, Hospital for Special Surgery","place":["New 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