ArticleScientific reports2019
The role of nuclear factor erythroid-2-related factor 2 expression in radiocontrast-induced nephropathy.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Sirtuins in kidney homeostasis and disease: where are we now?Frontiers in endocrinology · 2024Review
- Signal pathways involved in contrast-induced acute kidney injury.Frontiers in physiology · 2024Review
- Research progress on animal models of contrast-induced acute kidney injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- A novel contrast-induced acute kidney injury mouse model based on low-osmolar contrast medium.Renal failure · 2022Article
- The Pathophysiology and the Management of Radiocontrast-Induced Nephropathy.Diagnostics (Basel, Switzerland) · 2022Review
- Capsaicin Prevents Contrast-Associated Acute Kidney Injury through Activation of Nrf2 in Mice.Oxidative medicine and cellular longevity · 2022Article
- Systemic Immune-Inflammation Index Predicts Contrast-Induced Acute Kidney Injury in Patients Undergoing Coronary Angiography: A Cross-Sectional Study.Frontiers in medicine · 2022Article
- Pro-Inflammatory Serum Amyloid a Stimulates Renal Dysfunction and Enhances Atherosclerosis in Apo E-Deficient Mice.International journal of molecular sciences · 2021Article
- Article
- The Role of Sirtuins in Kidney Diseases.International journal of molecular sciences · 2020Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiocontrast-induced nephropathy (CIN) is the third most common cause of acute renal failure. The pathophysiology of CIN is related to tubular injury caused by oxidative stress, and nuclear factor erythroid-2-related factor 2 (Nrf2) is critical in coordinating intracellular antioxidative processes. We thus investigated the role of Nrf2 in CIN. CIN was established in mice and in NRK-52E cells via iohexol administration according to the protocols of previous studies. To determine the role of Nrf2 in CIN, Nrf2 expression was reduced in vivo using Nrf2 knockout (KO) mice (B6.129 × 1-Nfe2 l2tm1Ywk/J) and in vitro with siRNA treatment targeting Nrf2. Increased Nrf2 expression was observed after iohexol treatment both in vivo and in vitro. Serum creatinine at 24 h after iohexol injection was significantly higher in KO mice than in wild-type (WT) mice. Histologic examination showed that iohexol-induced tubular vacuolization and structural disruption were aggravated in Nrf2 KO mice. Significant increases in apoptosis and F4/80(+) inflammatory cell infiltration were demonstrated in KO mice compared to WT mice. In addition, the increase in reactive oxygen species after iohexol treatment was augmented by Nrf2 inhibition both in vivo and in vitro. Nrf2 may be implicated in the pathogenesis of CIN via the modulation of antioxidant, anti-apoptotic, and anti-inflammatory processes.
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