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Here, we address this challenge by engineering a dual\u2010functional metal\u2010ion\/L\u2010serine nanoarchitecture integrating two key components: precise kidney targeting via L\u2010serine's molecular recognition of the injury biomarker kidney injury molecule\u20101 (Kim\u20101), and bioinspired antioxidant catalysis through metal\u2010ion\/amino\u2010acid\u2010coordinated enzyme mimicry. Through systematic screening of metal ions (Mg\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    , Ca\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    , Mn\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    , Fe\n                    <jats:sup>3+<\/jats:sup>\n                    , Co\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    , Cu\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    , and Ce\n                    <jats:sup>3+<\/jats:sup>\n                    ), we identified Mn\u2010chelating L\u2010serine (L\u2010SerMn) as the optimal nanoarchitecture, displaying robust superoxide dismutase (SOD)\u2010 and catalase (CAT)\u2010like activities. Molecular dynamics simulations revealed stronger binding affinity of L\u2010SerMn to Kim\u20101 compared to free L\u2010serine. In vitro, L\u2010SerMn protected renal tubular epithelial cells from hypoxia\/reoxygenation (H\/R)\u2010induced damage by\u00a0functioning as a dual SOD\/CAT mimic. In vivo, L\u2010SerMn achieved selective accumulation in injured kidneys via Kim\u20101\u2010mediated targeting, enabling sustained restoration of redox homeostasis that ameliorated renal pathological injury. Mechanistically, L\u2010SerMn ameliorated renal I\/R injury and blocked the acute kidney injury (AKI)\u2010chronic kidney disease (CKD) transition via suppression of cellular senescence, through regulating the JAK2\u2010STAT3 and p53 signaling pathways. This work elegantly integrates coordination chemistry and biomimetic enzymology for the rational design of organ\u2010targeted nanotherapeutics, offering a promising strategy against ischemic diseases.\n                  <\/jats:p>","DOI":"10.1002\/anie.4618875","type":"journal-article","created":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T14:03:55Z","timestamp":1778249035000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Manganese\u2010Chelating L\u2010Serine Nanoarchitectures: Targeting Kidney Injury Molecule\u20101 for Reversing Renal Ischemia\u2010Reperfusion Injury via Senescence Regulation"],"prefix":"10.1002","volume":"65","author":[{"given":"Huajun","family":"Li","sequence":"first","affiliation":[{"name":"School of Traditional Chinese Medicine Faculty of Medicine Yangzhou University  Yangzhou Jiangsu P. R. 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