ReviewCell communication and signaling : CCS2024
Role of ferroptosis in chronic kidney disease.
Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.
- Emerging Therapeutic Potential of Fisetin for Nephrotoxicity, Kidney Injury, and Nephropathy: A Systematic Review.Current diabetes reviews · 2026Pooled it
- Research hotspots and future trends in lipid metabolism in chronic kidney disease: a bibliometric and visualization analysis from 2004 to 2023.Frontiers in pharmacology · 2024Pooled it
- β-Thujaplicin Mobilizes Renal Tubular Iron to Alleviate Diabetic Kidney Disease.Renal failure · 2026Article
- SOCS2 Downregulation Is Associated with a Ferro-Aging-Related Transcriptomic Signature in Proximal Tubular Cells in Chronic Kidney Disease.Biomedicines · 2026Article
- Indoxyl Sulfate Promotes Vascular Calcification in Association with Oxidative Stress and Activation of ERK and Wnt/β-Catenin Signaling Pathways.International journal of molecular sciences · 2026Article
- Molecular mechanisms of iron metabolism and ferroptosis in cardiovascular diseases and intervention strategies targeting natural products (Review).Molecular medicine reports · 2026Review
- The inflammatory-autophagy-NETs axis in renal fibrosis: mechanistic crosstalk and pathological feed-forward amplification loops.Molecular and cellular biochemistry · 2026Review
- Frailty and outcomes in older adults hospitalized for epilepsy: a nationwide inpatient sample study.BMC geriatrics · 2026Article
- Chrysin mitigates ciprofloxacin-induced nephrotoxicity: associations with notch/HES1 signaling, inflammation, and a ferroptosis-related molecular signature.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Interactions between the gut microbiome and ferroptosis in degenerative diseases: Novel mechanisms and potential therapeutic strategies.Acta pharmaceutica Sinica. B · 2026Review
- Quercetin Attenuates Iron Overload-Induced Renal Injury via Activating Nrf2/xCT/GPX4 Signaling to Inhibit Ferroptosis.Life (Basel, Switzerland) · 2026Article
- Identification of Ferroptosis-Related Hub Genes and Immune Infiltration Landscape in Chronic Kidney Disease via Bioinformatics and Experimental Verification.Immunity, inflammation and disease · 2026Article
- Antioxidants rescue murine mesangial cells from docosahexaenoic acid-induced ferroptosis.Molecular and cellular pediatrics · 2026Article
- Programmed cell death in gouty nephropathy: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Integrated untargeted and targeted metabolomics combined with experimental validation reveal glutathione-related oxidative stress in pediatric IgA vasculitis nephritis.Frontiers in pharmacology · 2026Article
- Iron-Driven Ferroptosis in Diabetic Kidney Disease: From Molecular Mechanisms to Targeted Therapeutic Translation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Mechanistic Insights into the Ferroptosis-Regulating Effects of EF in the Treatment of Chronic Renal Failure.Current medicinal chemistry · 2026Article
- Iron metabolism and ferroptosis: druggable targets to delay the progression of lupus nephritis.American journal of physiology. Renal physiology · 2026Review
- Article
- Diagnostic and prognostic signatures of glomerular membrane dysregulation in immune nephropathies.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) has historically been a significant global health concern, profoundly impacting both life and well-being. In the process of CKD, with the gradual loss of renal function, the incidence of various life-threatening complications, such as cardiovascular diseases, cerebrovascular accident, infection and stroke, is also increasing rapidly. Unfortunately, existing treatments exhibit limited ability to halt the progression of kidney injury in CKD, emphasizing the urgent need to delve into the precise molecular mechanisms governing the occurrence and development of CKD while identifying novel therapeutic targets. Renal fibrosis, a typical pathological feature of CKD, plays a pivotal role in disrupting normal renal structures and the loss of renal function. Ferroptosis is a recently discovered iron-dependent form of cell death characterized by lipid peroxide accumulation. Ferroptosis has emerged as a potential key player in various diseases and the initiation of organ fibrosis. Substantial evidence suggests that ferroptosis may significantly contribute to the intricate interplay between CKD and its progression. This review comprehensively outlines the intricate relationship between CKD and ferroptosis in terms of iron metabolism and lipid peroxidation, and discusses the current landscape of pharmacological research on ferroptosis, shedding light on promising avenues for intervention. It further illustrates recent breakthroughs in ferroptosis-related regulatory mechanisms implicated in the progression of CKD, thereby providing new insights for CKD treatment. Video Abstract.
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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.