{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T10:03:38Z","timestamp":1790244218587,"version":"4.1.0"},"reference-count":62,"publisher":"MDPI AG","issue":"19","license":[{"start":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T00:00:00Z","timestamp":1790208000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["22K08318"],"award-info":[{"award-number":["22K08318"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]},{"award":["22K08318"],"award-info":[{"award-number":["22K08318"]}],"id":[{"id":"https:\/\/ror.org\/00hhkn466","id-type":"ROR","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007449","name":"Takeda Science Foundation","doi-asserted-by":"publisher","award":["2024065636"],"award-info":[{"award-number":["2024065636"]}],"id":[{"id":"10.13039\/100007449","id-type":"DOI","asserted-by":"publisher"}]},{"award":["2024065636"],"award-info":[{"award-number":["2024065636"]}],"id":[{"id":"https:\/\/ror.org\/02y123g31","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Int. J. Mol. Sci.","IJMS"],"abstract":"<jats:p>Acute kidney injury (AKI) is a critical clinical challenge for which effective pharmacological therapies remain limited. Inflammation and oxidative stress play central roles in its pathogenesis. Here, we investigated the effects of Stachybotrys microspora triprenyl phenol-44D (SMTP-44D), a soluble epoxide hydrolase inhibitor that, unlike its analog SMTP-7, lacks thrombolytic activity, in a mouse model of renal ischemia\u2013reperfusion (I\/R)-induced AKI. SMTP-44D was administered either during or prior to ischemia. SMTP-44D improved renal functional parameters, including blood urea nitrogen, serum creatinine, and fractional sodium excretion in both protocols, with a protocol-dependent difference in creatinine clearance. An attenuation of tubular morphological alterations was observed when SMTP-44D was administered during ischemia, whereas pre-ischemic administration failed to demonstrate apparent morphological improvement. Mechanistic analysis was conducted using the pre-ischemic administration protocol. Urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule 1 were significantly reduced. SMTP-44D also suppressed renal tumor necrosis factor alpha, interleukin-1 beta, and NADPH oxidase-1 levels. Collectively, these functional and molecular findings suggest that SMTP-44D provides anti-inflammatory and antioxidant renoprotection, while evidence supporting structural protection is lacking in the pre-ischemic administration protocol. SMTP-44D warrants further investigation as a potential therapeutic strategy for I\/R-induced AKI.<\/jats:p>","DOI":"10.3390\/ijms27198506","type":"journal-article","created":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T09:07:54Z","timestamp":1790240874000},"page":"8506","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["SMTP-44D Attenuates Renal Inflammatory\/Oxidative Dysfunction in a Mouse Model of Ischemia\u2013Reperfusion-Induced Acute Kidney Injury"],"prefix":"10.3390","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3935-8742","authenticated-orcid":false,"given":"Keita","family":"Shibata","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Graduate School of Pharmacy, Showa University, Tokyo 142-8555, Japan"},{"name":"Pharmacological Research Center, Showa Medical University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan"}],"role":[{"vocabulary":"crossref","role":"author"},{"role":"conceptualization","vocabulary":"credit"},{"role":"methodology","vocabulary":"credit"},{"role":"formal-analysis","vocabulary":"credit"},{"role":"investigation","vocabulary":"credit"},{"role":"data-curation","vocabulary":"credit"},{"role":"writing-original-draft","vocabulary":"credit"},{"role":"project-administration","vocabulary":"credit"},{"role":"funding-acquisition","vocabulary":"credit"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3340-7312","authenticated-orcid":false,"given":"Keiji","family":"Hasumi","sequence":"additional","affiliation":[{"name":"Department of Applied Biological Science, Tokyo University of Agriculture and Technology, 3-5-8 Saiwaicho, Fuchu, Tokyo 183-8509, Japan"},{"name":"Division of Research and Development, TMS Co., Ltd., Fuchu, Tokyo 183-0055, Japan"}],"role":[{"vocabulary":"crossref","role":"author"},{"role":"resources","vocabulary":"credit"},{"role":"writing-review-editing","vocabulary":"credit"},{"role":"supervision","vocabulary":"credit"}]},{"given":"Koji","family":"Nobe","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Graduate School of Pharmacy, Showa University, Tokyo 142-8555, Japan"},{"name":"Pharmacological Research Center, Showa Medical University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan"}],"role":[{"vocabulary":"crossref","role":"author"},{"role":"writing-review-editing","vocabulary":"credit"},{"role":"supervision","vocabulary":"credit"}]}],"member":"1968","published-online":{"date-parts":[[2026,9,24]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1482","DOI":"10.1016\/j.athoracsur.2016.04.020","article-title":"Acute Kidney Injury Severity and Long-Term Readmission and Mortality After Cardiac Surgery","volume":"102","author":"Brown","year":"2016","journal-title":"Ann. 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