ReviewRenal failure2025
The role of ferroptosis in acute kidney injury: the preemptive mode of cell death and the bridging effect.
Review in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- The lactate-lactylation axis in acute kidney injury: mechanisms from metabolic reprogramming to epigenetic regulation and clinical therapeutic prospects.International urology and nephrology · 2026Review
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Programmed cell death in kidney disease: integrated crosstalk among ferroptosis, pyroptosis, apoptosis, and cuproptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Chrysophanol ameliorates ferroptosis in acute kidney injury by promoting SIRT3-mediated NRF2 deacetylation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Methylmalonic acid as a ferroptosis-derived danger signal: activation of the PI3K-NF-κB pathway drives M1 macrophage polarization in renal ischemia-reperfusion injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Research Progress on the Treatment of Renal Injury with Esculetin: Multi-Target Pharmacological Mechanism and Clinical Translation Prospect.International journal of molecular sciences · 2026Review
- Growth Differentiation Factor 15 (GDF15) Protects Against Sepsis-Associated Acute Kidney Injury via Suppression of TLR4-MyD88-NF-κB Signaling and Ferroptosis.BioFactors (Oxford, England)Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis represents a distinctive mechanism of cell death, differing from necroptosis, necrosis, and apoptosis. It is triggered by the accumulation of lipid peroxides, driven by iron-catalyzed reactions. This oxidative damage is essential for triggering the ferroptotic pathway. Compared with apoptosis and necroptosis, ferroptosis is activated earlier in acute kidney injury (AKI), serving as a preemptive mechanism of cell death. Ferroptosis acts as a link between synchronous waves of renal tubular cell death by triggering cell death amplification loops and connects cell damage with inflammatory responses, thus constituting a crucial stage in the progression of AKI. This paper discusses the mechanisms that trigger ferroptosis in AKI and how ferroptosis, as a preemptive mode of cell death, exacerbates AKI through ferroptotic waves, modulates inflammatory responses, triggering apoptosis, necroptosis, and pyroptosis.
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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.