{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T14:27:23Z","timestamp":1782397643020,"version":"3.54.5"},"reference-count":81,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2024,7,26]],"date-time":"2024-07-26T00:00:00Z","timestamp":1721952000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2024,7,26]],"date-time":"2024-07-26T00:00:00Z","timestamp":1721952000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Renal ischaemia and reperfusion (I\/R) is caused by a sudden temporary impairment of the blood flow. I\/R is a prevalent cause of acute kidney injury. As nitric oxide generated by inducible nitric oxide synthase (iNOS) has detrimental effects during I\/R, the pharmacological blockade of iNOS has been proposed as a potential strategy to prevent I\/R injury. The aim of this study was to improve the understanding of 1400W (an iNOS inhibitor) on renal I\/R as a pharmacological strategy against kidney disease. BALB\/c mice received 30\u00a0min of bilateral ischaemia, followed by 48\u00a0h or 28\u00a0days of reperfusion. Vehicle or 1400W (10\u00a0mg\/kg) was administered 30\u00a0min before inducing ischaemia. We found that after 48\u00a0h of reperfusion 1400W decreased the serum creatinine, blood urea nitrogen, neutrophil gelatinase\u2010associated lipocalin and proliferating cell nuclear antigen 3 in the I\/R animals. Unexpectedly, we observed mRNA upregulation of genes involved in kidney injury, cell\u2010cycle arrest, inflammation, mesenchymal transition and endothelial activation in the renal medulla of sham animals treated with 1400W. We also explored if 1400W promoted chronic kidney dysfunction 28\u00a0days after I\/R and did not find significant alterations in renal function, fibrosis, blood pressure or mortality. The results provide evidence that 1400W may have adverse effects in the renal medulla. Importantly, our data point to 1400W\u2010induced endothelial dysfunction, establishing therapeutic limitations for its use.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16186-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Acute kidney injury is a global health problem associated with high morbidity and mortality.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The pharmacological blockade of inducible nitric oxide synthase (iNOS) has been proposed as a potential strategy to prevent AKI induced by ischaemia and reperfusion (I\/R).<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Our main finding is that 1400W, a selective and irreversible iNOS inhibitor with low toxicity that is proposed as a therapeutic strategy to prevent kidney I\/R injury, produces aberrant gene expression in the medulla associated to tissue injury, cell cycle arrest, inflammation, mesenchymal transition and endothelial activation.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The negative effect of 1400W observed in the renal medulla at 48\u00a0h from drug administration, is transient as it did not translate into a chronic kidney disease condition.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp285944","type":"journal-article","created":{"date-parts":[[2024,7,26]],"date-time":"2024-07-26T08:45:20Z","timestamp":1721983520000},"page":"4279-4301","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["The protective effect of 1400W against ischaemia and reperfusion injury is countered by transient medullary kidney endothelial dysregulation"],"prefix":"10.1113","volume":"604","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2602-1147","authenticated-orcid":false,"given":"Consuelo","family":"Pasten","sequence":"first","affiliation":[{"name":"Centro de Investigaci\u00f3n e Innovaci\u00f3n Biom\u00e9dica (CiiB), Programa de Fisiolog\u00eda, Laboratorio de Fisiolog\u00eda Integrativa y 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