{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T04:19:33Z","timestamp":1787717973447,"version":"build-2784847793"},"reference-count":43,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T00:00:00Z","timestamp":1785888000000},"content-version":"vor","delay-in-days":35,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Diabetes"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Diabetic nephropathy (DN) is a leading cause of end\u2010stage renal disease. ELAVL1, an RNA\u2010binding protein, is involved in the regulation of genes closely associated with DN pathogenesis, whereas suPAR acts as a circulating mediator that promotes podocyte damage and contributes to proteinuric kidney disorders. However, whether ELAVL1 regulates suPAR release in DN remains unexplored.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Clinical samples from patients with DN were collected and analyzed. In\u00a0vitro, podocytes were treated with high glucose, and ELAVL1 or PLAUR (encoding uPAR) was knocked down or overexpressed using lentiviral transduction. In db\/db mice, podocyte\u2010specific manipulation of Elavl1 or Plaur was performed via adeno\u2010associated virus\u2010mediated delivery. Renal function was assessed by measuring the urinary albumin\u2010to\u2010creatinine ratio (UACR) and serum creatinine. Glomerular pathology and inflammatory markers were evaluated histologically and biochemically.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>ELAVL1 was upregulated in DN and positively correlated with podocyte injury. Knockdown of ELAVL1 mitigated hyperglycemia\u2010induced podocyte damage and inflammatory responses. Mechanistically, ELAVL1 directly bound to and stabilized PLAUR mRNA, leading to increased uPAR protein expression and elevated suPAR secretion. The protective effects of ELAVL1 knockdown were reversed by PLAUR overexpression in podocytes. In diabetic mice, podocyte\u2010specific knockdown of Elavl1 or Plaur markedly lowered circulating suPAR levels and alleviated renal dysfunction and histopathological injury. Moreover, restoration of the PLAUR\u2010suPAR axis abolished the renoprotective benefits conferred by Elavl1 knockdown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Hyperglycemia\u2010induced ELAVL1 upregulates PLAUR and suPAR release from podocytes, promoting renal inflammation and injury. Targeting the ELAVL1\u2010PLAUR\u2010suPAR axis may offer a therapeutic strategy for DN.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/1753-0407.70254","type":"journal-article","created":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T00:31:22Z","timestamp":1785976282000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The\n                    <scp>ELAVL1<\/scp>\n                    \u2010\n                    <scp>PLAUR<\/scp>\n                    \u2010\n                    <scp>suPAR<\/scp>\n                    Axis Exacerbates Diabetic Nephropathy by Promoting Podocyte Injury and Inflammation"],"prefix":"10.1111","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-1334-9321","authenticated-orcid":false,"given":"DanDan","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Nephrology Henan Provincial People's Hospital  Zhengzhou City Henan Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liang","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Nephrology Henan Provincial People's Hospital  Zhengzhou City Henan Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"LinLin","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Nephrology Henan Provincial People's Hospital  Zhengzhou City Henan Province 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