{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T13:19:37Z","timestamp":1790601577430,"version":"4.1.0"},"reference-count":117,"publisher":"MDPI AG","issue":"15","license":[{"start":{"date-parts":[[2022,7,31]],"date-time":"2022-07-31T00:00:00Z","timestamp":1659225600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Taipei Medical University, Taiwan","award":["110TMU-WFH-18"],"award-info":[{"award-number":["110TMU-WFH-18"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Preterm birth interrupts the development and maturation of the kidneys during the critical growth period. The kidneys can also exhibit structural defects and functional impairment due to hyperoxia, as demonstrated by various animal studies. Furthermore, hyperoxia during nephrogenesis impairs renal tubular development and induces glomerular and tubular injuries, which manifest as renal corpuscle enlargement, renal tubular necrosis, interstitial inflammation, and kidney fibrosis. Preterm birth along with hyperoxia exposure induces a pathological predisposition to chronic kidney disease. Hyperoxia-induced kidney injuries are influenced by several molecular factors, including hypoxia-inducible factor-1\u03b1 and interleukin-6\/Smad2\/transforming growth factor-\u03b2, and Wnt\/\u03b2-catenin signaling pathways; these are key to cell proliferation, tissue inflammation, and cell membrane repair. Hyperoxia-induced oxidative stress is characterized by the attenuation or the induction of multiple molecular factors associated with kidney damage. This review focuses on the molecular pathways involved in the pathogenesis of hyperoxia-induced kidney injuries to establish a framework for potential interventions.<\/jats:p>","DOI":"10.3390\/ijms23158492","type":"journal-article","created":{"date-parts":[[2022,8,1]],"date-time":"2022-08-01T02:06:42Z","timestamp":1659319602000},"page":"8492","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Kidney Injuries and Evolution of Chronic Kidney Diseases Due to Neonatal Hyperoxia Exposure Based on Animal Studies"],"prefix":"10.3390","volume":"23","author":[{"given":"Liang-Ti","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan"},{"name":"Department of Pediatrics, School of Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8762-8957","authenticated-orcid":false,"given":"Chung-Ming","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan"},{"name":"Department of Pediatrics, Taipei Medical University Hospital, Taipei 110, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2022,7,31]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"l1346","DOI":"10.1136\/bmj.l1346","article-title":"Preterm birth and risk of chronic kidney disease from childhood into midadulthood: National cohort study","volume":"365","author":"Crump","year":"2019","journal-title":"BMJ"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"68","DOI":"10.1016\/j.siny.2015.12.011","article-title":"The epidemiology, etiology, and costs of preterm birth","volume":"21","author":"Frey","year":"2016","journal-title":"Semin. 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