{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T07:50:03Z","timestamp":1785829803196,"version":"3.56.0"},"reference-count":26,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,2,15]],"date-time":"2026-02-15T00:00:00Z","timestamp":1771113600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,2,15]],"date-time":"2026-02-15T00:00:00Z","timestamp":1771113600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004935","name":"S\u00fcleyman Demirel \u00dcniversitesi","doi-asserted-by":"publisher","award":["9524"],"award-info":[{"award-number":["9524"]}],"id":[{"id":"10.13039\/501100004935","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Applied Toxicology"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Methotrexate (MTX), a common chemotherapeutic and immunosuppressive drug, is limited by dose\u2010dependent nephrotoxicity mediated by oxidative stress, mitochondrial dysfunction, and apoptosis. L\u2010carnitine (LCR), a mitochondrial cofactor with antioxidant and anti\u2010apoptotic properties, may counteract these mechanisms. This study aims to determine whether LCR mitigates MTX\u2010induced nephrotoxicity by rebalancing the BAX\/BCL2 apoptotic axis and preserving renal compartment integrity (endothelial CD31, tubular cytokeratin, podocyte WT1). Twenty\u2010four female Wistar rats were randomized into Control, MTX (20\u2009mg\/kg, i.p., Day 5), LCR (200\u2009mg\/kg\/day, i.p., 10\u2009days), and MTX\u2009+\u2009LCR groups (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20096 each). Renal injury was assessed by serum creatinine, urea, BUN, histopathology, immunohistochemistry (CD31, cytokeratin, WT1), and RT\u2010qPCR for BAX\/BCL2. MTX impaired renal function, caused vascular hyperemia, hemorrhage, and tubular necrosis, increased CD31, cytokeratin, and BAX and decreased WT1 and BCL2. LCR co\u2010treatment improved biochemical indices, reduced lesions, decreased CD31 and cytokeratin, partially restored WT1 and re\u2010balanced apoptosis (BAX\u2193, BCL2\u2191). LCR disrupts oxidative stress, the mitochondrial apoptosis cascade, and preserves endothelial, tubular, and podocyte integrity in MTX nephrotoxicity.\n                  <\/jats:p>","DOI":"10.1002\/jat.70096","type":"journal-article","created":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T02:44:02Z","timestamp":1771209842000},"page":"3102-3112","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["L\u2010Carnitine Attenuates Methotrexate\u2010Induced Nephrotoxicity by Modulating BAX\/BCL2 Apoptotic Signaling and Preserving Podocyte, Endothelial, and Tubular Integrity"],"prefix":"10.1002","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7712-2899","authenticated-orcid":false,"given":"\u00d6zlem","family":"T\u00fcrkoglu","sequence":"first","affiliation":[{"name":"Department of Radiology, Hamidiye Faculty of Medicine University of Health Sciences  \u0130stanbul 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