{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T09:12:05Z","timestamp":1790327525933,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T00:00:00Z","timestamp":1789689600000},"content-version":"vor","delay-in-days":17,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"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":["82472198"],"award-info":[{"award-number":["82472198"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82672824"],"award-info":[{"award-number":["82672824"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82430069"],"award-info":[{"award-number":["82430069"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["32370711"],"award-info":[{"award-number":["32370711"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical & Translational Med"],"published-print":{"date-parts":[[2026,9]]},"abstract":"Abstract<\/jats:title>\n \n Background<\/jats:title>\n Sepsis\u2010associated acute kidney injury (S\u2010AKI) imposes substantial morbidity and mortality burdens in critically ill populations. This study aimed to construct a spatiotemporal multi\u2010omics atlas of kidneys in a mouse model of S\u2010AKI using spatial metabolomics and proteomics, and to explore potential therapeutic targets for S\u2010AKI.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n A spatiotemporal multi\u2010omics atlas of S\u2010AKI mouse kidneys was constructed using spatial metabolomics and proteomics. Arginine metabolism was evaluated via L\u2010arginine supplementation. ARG2 was inhibited by nor\u2010NOHA or renal tubule\u2010specific knockdown. Kidney injury was assessed by histopathology, real\u2010time glomerular filtration rate (RT\u2010GFR), serum serum urea nitrogen (BUN), and injury markers. RNA\u2010seq and serum metabolomics elucidated nor\u2010NOHA's mechanism, with in vivo verification of pathway activation and lipid reduction. In vitro studies used ARG2 KO renal primary tubular epithelial cells (RPTCs) and kidney organoids.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n Arginine metabolism played a crucial role, but L\u2010arginine supplementation did not improve renal function. ARG2 was significantly upregulated in proximal and distal tubules of the renal outer medulla and in macrophages. Treatment with the arginase inhibitor nor\u2010NOHA or knockdown of ARG2 in renal tubules significantly alleviated kidney injury, as evidenced by reduced tubular injury, increased RT\u2010GFR, decreased BUN, and reduced injury markers. RNA\u2010seq and serum metabolomics showed that nor\u2010NOHA significantly reduced lipid accumulation in renal tubules and serum, with significant enrichment of the peroxisome proliferator\u2010activated receptor (PPAR) pathway centered around PPAR\u03b3. In vivo experiments confirmed pathway activation and alleviation of lipid accumulation. In vitro experiments using RPTCs from ARG2 knockout mice and human kidney organoid model revealed that ARG2 knockout restored PPAR\u03b3 expression and reduced tubular lipid accumulation.<\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Inhibiting ARG2 in renal tubules during S\u2010AKI may alleviate lipid accumulation and kidney injury by activating PPAR\u03b3, providing a new therapeutic strategy.<\/jats:p>\n <\/jats:sec>\n \n Key points<\/jats:title>\n \n \n \n Spatiotemporal multi\u2010omics analysis constructed a detailed atlas of S\u2010AKI kidneys, revealing the regional specificity of metabolic and protein expression in different kidney regions during the progression from sepsis to S\u2010AKI.<\/jats:p>\n <\/jats:list-item>\n \n Arginine metabolism plays a key role in the pathogenesis of S\u2010AKI, with arginine levels continuously decreasing in S\u2010AKI and significantly correlating with renal function.<\/jats:p>\n <\/jats:list-item>\n \n In S\u2010AKI, ARG2 expression increases, mainly localizing to renal tubular cells and macrophages. Renal tubule\u2014specific ARG2 knockdown reduces renal tubular lipid accumulation and kidney injury in S\u2010AKI, likely playing an important role by regulating PPAR\u03b3 to affect lipid accumulation.<\/jats:p>\n <\/jats:list-item>\n \n The kidney organoids with ARG2 knockout further confirmed the key role of ARG2 in S\u2010AKI, providing a new therapeutic target for S\u2010AKI treatment.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/ctm2.70770","type":"journal-article","created":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T15:37:07Z","timestamp":1789745827000},"source":"Crossref","is-referenced-by-count":0,"title":["Arginase 2 deficiency mitigates sepsis\u2010associated acute kidney injury by alleviating lipid accumulation"],"prefix":"10.1002","volume":"16","author":[{"given":"Yu","family":"Xin","sequence":"first","affiliation":[{"name":"Department of Critical Care Medicine the First Affiliated Hospital of Harbin Medical 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