ArticleOxidative medicine and cellular longevity2020
Neonatal Hyperoxia Downregulates Claudin-4, Occludin, and ZO-1 Expression in Rat Kidney Accompanied by Impaired Proximal Tubular Development.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Neonatal kidney injury in the hyperoxia-induced bronchopulmonary dysplasia mouse models: effect on morphology and biomarkers.Pediatric research · 2026Article
- Correction to "Neonatal Hyperoxia Downregulates Claudin-4, Occludin, and ZO-1 Expression in Rat Kidney Accompanied by Impaired Proximal Tubular Development".Oxidative medicine and cellular longevity · 2026Article
- Does hypoxemia aggravate sepsis-associated acute kidney injury? Integrated clinical and experimental evidence.Intensive care medicine experimental · 2025Article
- The effect of NF-kB and MAPK mediated Proinflammatory microenvironment on renal aging and amyloid deposition in elder rats.Scientific reports · 2025Article
- LeechWorld journal of gastroenterology · 2024Article
- The danger of hyperoxia on the rat kidneys: is tadalafil a real shield?International urology and nephrology · 2023Article
- Kidney Injuries and Evolution of Chronic Kidney Diseases Due to Neonatal Hyperoxia Exposure Based on Animal Studies.International journal of molecular sciences · 2022Review
- Hyperoxia and Acute Kidney Injury: A Tale of Oxygen and the Kidney.Seminars in nephrology · 2022Review
- Matrix Metalloproteinase-10 in Kidney Injury Repair and Disease.International journal of molecular sciences · 2022Review
- Anti-Tn Monoclonal Antibody Ameliorates Hyperoxia-Induced Kidney Injury by Suppressing Oxidative Stress and Inflammation in Neonatal Mice.Mediators of inflammation · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperoxia is essential to manage in preterm infants but causes injury to immature kidney. Previous study indicates that hyperoxia causes oxidative damage to neonatal kidney and impairs renal development. However, the underlying mechanisms by which neonatal hyperoxia effects on immature kidney still need to be elucidated. Tight junction, among which the representative proteins are claudin-4, occludin, and ZO-1, plays a crucial role in nephrogenesis and maintaining renal function. Inflammatory cytokines are involved in the pleiotropic regulation of tight junction proteins. Here, we investigated how neonatal hyperoxia affected the expression of key tight junction proteins and inflammatory factors (IL-6 and TNF-
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