ArticleJournal of molecular histology2025
FGF5 alleviates ferroptosis in renal tubular epithelial cells by inducing mitophagy under in vitro ischemia-reperfusion-like injury.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- Chasing the FoxO in Metabolic Disorders: Novel Considerations for Oxidative Stress, Programmed Cell Death, Wnt, and the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Review
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Mitophagy in kidney and lung epithelial cells: molecular mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Renal ischemic disease represents a severe clinical pathological condition commonly observed in acute kidney injury (AKI), renal transplantation, and kidney surgery. It leads to renal tubular epithelial cell damage, inflammatory responses, and cell death, potentially progressing to chronic kidney disease (CKD) or even renal failure, significantly impairing patients' quality of life and survival rates. Current therapeutic strategies for renal ischemia-reperfusion injury (IRI) include pharmacological interventions, cell therapy, and gene therapy, yet their efficacy remains limited and may be accompanied by adverse effects. Thus, there is an urgent need to explore novel therapeutic targets and strategies. Fibroblast growth factor 5 (FGF5), a key member of the FGF family, plays crucial roles in cell proliferation, differentiation, and tissue repair. However, its specific mechanism in renal IRI remains unclear. This study aimed to investigate the therapeutic effects of FGF5 on renal IRI and its underlying molecular mechanisms in vitro. Using normal rat kidney-52E (NRK-52E) and human kidney-2 (HK-2 cell) models, we evaluated the impact of FGF5 on cell viability, oxidative stress, inflammatory responses, and renal cell death. Our findings demonstrate that FGF5 exhibits significant biological activity and further reveal its regulatory role in suppressing ferroptosis through activation of the Mitophagy. In conclusion, this study identifies FGF5 as a potential therapeutic agent for renal IRI and provides a theoretical foundation for developing FGF5-based treatment strategies. These findings hold substantial scientific and clinical value, potentially opening new avenues for treating renal ischemic diseases.
Indexed as
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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.