{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T07:25:53Z","timestamp":1786951553500,"version":"build-2736575974"},"reference-count":42,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T00:00:00Z","timestamp":1785715200000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100003453","name":"Natural Science Foundation of Guangdong Province","doi-asserted-by":"publisher","award":["2025A1515012666"],"award-info":[{"award-number":["2025A1515012666"]}],"id":[{"id":"10.13039\/501100003453","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Hyperuricaemia (HUA) is a recognized risk factor for cardiovascular and renal diseases. Isobavachin, a dihydroflavone derivative, demonstrates significant efficacy in reducing uric acid levels. This study investigated the nephroprotective and cardioprotective effects and molecular mechanisms of isobavachin. Through integrative network pharmacology, pathway enrichment analysis, and molecular docking, NF\u2010\u03baB was identified as a potential target of isobavachin in the context of hyperuricemia\u2010related cardiac and renal injury. Isobavachin treatment inhibited the activation of the NF\u2010\u03baB pathway, leading to cytoprotection in uric acid (UA)\u2010stimulated mRTEC and H9C2 cells. In chronic HUA mice, isobavachin treatment significantly improved renal pathology and reduced renal collagen deposition by inhibiting epithelial\u2010to\u2010mesenchymal transition. Isobavachin administration demonstrated therapeutic efficacy in attenuating myocardial injury, hypertrophy, and fibrotic remodeling. Notably, the anti\u2010inflammatory effects of isobavachin were particularly evident in both renal and cardiac tissues, primarily mediated through its dual regulatory capacity in suppressing NF\u2010\u03baB pathway activation and NLRP3 inflammasome formation. In conclusion, isobavachin ameliorated cardiac and renal damage caused by chronic HUA, suggesting a new strategy to prevent HUA.<\/jats:p>","DOI":"10.1002\/jbt.71058","type":"journal-article","created":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T18:23:56Z","timestamp":1785781436000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Isobavachin Attenuates Renal and Cardiac Injury in Chronic Hyperuricemia via Modulation of NF\u2010\u03baB and NLRP3 Signaling Pathways"],"prefix":"10.1002","volume":"40","author":[{"given":"Yongmei","family":"Li","sequence":"first","affiliation":[{"name":"Dongguan Key Laboratory of Precision Drug Individualized Therapy, Department of Clinical Pharmacy, The Affiliated Dongguan Songshan Lake Central Hospital Guangdong Medical University Dongguan China"},{"name":"NMPA Key Laboratory for Research and Evaluation of Drug Metabolism &amp; Guangdong\u2010Hongkong\u2010Macao Joint Laboratory for New Drug Screening, School of Pharmaceutical Sciences Southern Medical University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuexin","family":"Xu","sequence":"additional","affiliation":[{"name":"NMPA Key Laboratory for Research and Evaluation of Drug Metabolism &amp; 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