{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T21:30:32Z","timestamp":1793223032005,"version":"4.5.0"},"reference-count":61,"publisher":"Wiley","issue":"26","license":[{"start":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T00:00:00Z","timestamp":1772496000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T00:00:00Z","timestamp":1772496000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82474175"],"award-info":[{"award-number":["82474175"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    The transition from acute kidney injury (AKI) to chronic kidney disease (CKD) lacks effective therapies. Using a murine aristolochic acid I model (AAI), followed by a 2 week remodeling phase, we mapped macrophage states across the AKI to CKD transition. Single\u2010cell RNA sequencing of kidneys from control, acute, and remodeling stages profiled 39\u00a0345 cells spanning 18 clusters. Macrophage subclustering and trajectories revealed emergence of scar\u2010associated macrophages (SMs) marked by high Acp5 (encoding tartrate\u2010resistant acid phosphatase 5 (TRAP5)) and enriched during the remodeling phase. Cell\u2013cell communication highlighted a dominant Spp1\u2013Cd44 axis driving SM activation. Immunofluorescence confirmed TRAP5\n                    <jats:sup>+<\/jats:sup>\n                    CD68\n                    <jats:sup>+<\/jats:sup>\n                    macrophage accumulation in multiple murine CKD and human CKD biopsies.\n                  <\/jats:p>\n                  <jats:p>Functionally, pharmacological TRAP5 inhibition conferred robust protection against AKI\u2013CKD transition. TRAP5 blockade initiated in the AKI phase markedly attenuated fibrosis, inflammation, and renal dysfunction in both AAI and ischemia\u2010reperfusion injury (IRI) models; while preinhibition similarly mitigated unilateral ureteral obstruction (UUO)\u2010induced fibrosis. In bone marrow\u2010derived macrophages (BMDMs), TRAP5 blockade abrogated osteopontin (Spp1)\u2010driven metabolic and profibrotic reprogramming.<\/jats:p>\n                  <jats:p>\n                    In conclusion, TRAP5\n                    <jats:sup>+<\/jats:sup>\n                    scar\u2010associated macrophages are disease\u2010promoting effectors of maladaptive remodeling in AKI\u2013CKD transition. Targeting TRAP5 not only suppresses profibrotic macrophage activation but also protects renal structure and function across multiple models, establishing TRAP5 inhibition as a promising therapeutic strategy to halt CKD progression.\n                  <\/jats:p>","DOI":"10.1002\/advs.202519855","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T11:33:41Z","timestamp":1772969621000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["TRAP5 Inhibition Targeting Scar\u2010Associated Macrophages Ameliorates Acute Kidney Injury to Chronic Kidney Disease Transition"],"prefix":"10.1002","volume":"13","author":[{"given":"Chenxi","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Nephrology Yueyang Hospital of Integrated Traditional Chinese and Western Medicine Shanghai University of Traditional Chinese Medicine  Shanghai 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