{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T18:06:04Z","timestamp":1790877964232,"version":"4.1.0"},"reference-count":50,"publisher":"American Physiological Society","issue":"6","funder":[{"name":"The Korea Health Technology R&D Project","award":["HI15C2212"],"award-info":[{"award-number":["HI15C2212"]}]},{"name":"Basic Science Research Program","award":["NRF-2015R1D1A4A01019877"],"award-info":[{"award-number":["NRF-2015R1D1A4A01019877"]}]},{"name":"The 2015 Research grant of Inje University Busan Paik Hospital","award":["Paik Hospital-2015"],"award-info":[{"award-number":["Paik Hospital-2015"]}]},{"name":"The 2017 creative research program of Inje University","award":["Inje University-2017"],"award-info":[{"award-number":["Inje University-2017"]}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"crossref","award":["NIH R35CA197442"],"award-info":[{"award-number":["NIH R35CA197442"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2020,12,1]]},"abstract":"<jats:p>\n                    In the present study, we demonstrated the marked activity of SW033291, an inhibitor of 15-hydoxyprostaglandin dehydrogenase (15-PGDH), in preventing acute kidney injury (AKI) in a murine model of ischemia-reperfusion injury. AKI due to ischemic injury represents a significant clinical problem. PGE\n                    <jats:sub>2<\/jats:sub>\n                    is vasodilatory in the kidney, but it is rapidly degraded in vivo due to catabolism by 15-PGDH. We investigated the potential of SW033291, a potent and specific 15-PGDH inhibitor, as prophylactic treatment for ischemic AKI. Prophylactic administration of SW033291 significantly increased renal tissue PGE\n                    <jats:sub>2<\/jats:sub>\n                    levels and increased post-AKI renal blood flow and renal arteriole area. In parallel, prophylactic SW033291 decreased post-AKI renal morphology injury scores and tubular apoptosis and markedly reduced biomarkers of renal injury that included blood urea nitrogen, creatinine, neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1. Prophylactic SW033291 also reduced post-AKI induction of proinflammatory cytokines, high-mobility group box 1, and malondialdehyde. Protective effects of SW033291 were mediated by PGE\n                    <jats:sub>2<\/jats:sub>\n                    signaling, as they could be blocked by pharmacological inhibition of PGE\n                    <jats:sub>2<\/jats:sub>\n                    synthesis. Consistent with activation of PGE\n                    <jats:sub>2<\/jats:sub>\n                    signaling, SW033291 induced renal levels of both EP\n                    <jats:sub>4<\/jats:sub>\n                    receptors and cAMP, along with other vasodilatory effectors, including AMP, adenosine, and the adenosine A\n                    <jats:sub>2A<\/jats:sub>\n                    receptor. The protective effects of SW0333291 could largely be achieved with a single prophylactic dose of the drug. Inhibition of 15-PGDH may thus represent a novel strategy for prophylaxis of ischemic AKI in multiple clinical settings, including renal transplantation and cardiovascular surgery.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00103.2020","type":"journal-article","created":{"date-parts":[[2020,11,2]],"date-time":"2020-11-02T06:54:20Z","timestamp":1604300060000},"page":"F1054-F1066","source":"Crossref","is-referenced-by-count":22,"title":["Inhibition of 15-PGDH prevents ischemic renal injury by the PGE\n                    <sub>2<\/sub>\n                    \/EP\n                    <sub>4<\/sub>\n                    signaling pathway mediating vasodilation, increased renal blood flow, and increased adenosine\/A\n                    <sub>2A<\/sub>\n                    receptors"],"prefix":"10.1152","volume":"319","author":[{"given":"Hye Jung","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Surgery, Busan Paik Hospital, Inje University College of Medicine, Busan, Republic of Korea"},{"name":"Paik Institute for Clinical Research, Inje University College of Medicine, Busan, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sun-Hee","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Surgery, Busan Paik Hospital, Inje University College of Medicine, Busan, Republic of Korea"},{"name":"In-Dang Bio Medical Research Institute, Busan Paik Hospital, Inje University College of Medicine, Busan, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minjung","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Surgery, Busan Paik Hospital, Inje University College of Medicine, Busan, Republic of Korea"},{"name":"Paik Institute for Clinical Research, Inje University College of Medicine, Busan, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"HyungJoo","family":"Baik","sequence":"additional","affiliation":[{"name":"Department of Surgery, Busan Paik Hospital, Inje University College of Medicine, Busan, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seok Ju","family":"Park","sequence":"additional","affiliation":[{"name":"Paik Institute for Clinical Research, Inje University College of Medicine, Busan, Republic of Korea"},{"name":"Department of Nephrology, Busan Paik Hospital, Inje University College of Medicine, Busan, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mi Seon","family":"Kang","sequence":"additional","affiliation":[{"name":"Department of Pathology, Inje University College of Medicine, Busan, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong-Hyun","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, 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