ArticleAntioxidants (Basel, Switzerland)2025
Intermittent Fasting Protects Against the Progression from Acute Kidney Injury to Chronic Kidney Disease.
Article in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Review
- The Mechanisms and Treatment Approaches of Oxidative Stress and Inflammation in the Development of Chronic Kidney Disease.Current hypertension reviews · 2026Review
- Article
- Advances in Intermittent Fasting Applications for Critically Ill Patients.International journal of general medicine · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Acute kidney injury (AKI) is a major but often underestimated risk factor for the development of chronic kidney disease (CKD). Exploring innovative approaches to prevent this progression is critical. Intermittent fasting (IF), recognized for its metabolic and anti-inflammatory benefits, may offer protective effects in this context. Using a unilateral ischemia-reperfusion injury (UIRI) model in male C57BL/6 mice, we evaluated the impact of IF on tubulointerstitial fibrosis and tubular epithelial-mesenchymal transition (EMT) over 8 weeks. Mice in the IF group followed a 5:2 regimen, fasting for 24 h twice weekly. Four groups were studied: control, IF, UIRI, and IF + UIRI. The UIRI group exhibited increased fibrosis and EMT, both of which were significantly attenuated in the IF + UIRI group. IF also reduced levels of TGF-β1, phosphorylated NF-κB p65, inflammatory cytokines, and F4/80-positive macrophages, along with markers of oxidative stress. These findings highlight IF's ability to mitigate fibrosis and EMT through reductions in inflammation and oxidative stress during AKI-to-CKD progression. Our study suggests that IF may serve as a promising dietary strategy to prevent AKI from advancing into CKD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.