ReviewMolecular biology reports2024
Ferroptosis and its emerging role in kidney stone formation.
Review in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Integrative transcriptomic and single-cell analyses identify CD74 as a candidate regulator of ferroptosis in renal tubular cells during nephrolithiasis.Renal failure · 2026Article
- Phenylalanine primes renal tubular redox vulnerability and calcium oxalate crystal retention through a PPARδ-CPT1A fatty-acid oxidation axis.Redox biology · 2026Article
- Per- and polyfluoroalkyl substances and kidney disease: Genetic associations and computational prioritization of candidate toxicogenomic pathways.PLoS computational biology · 2026Article
- Possible role of ribosome biogenesis in the recovery from transient hepatic damage caused by ethylene glycol in rats.Forensic toxicology · 2026Article
- Article
- ACAA1 mediates arachidonic acid dysregulation and membrane phospholipid remodeling to promote crystal-cell adhesion and ferroptosis susceptibility in calcium oxalate kidney stone.Journal of pharmaceutical analysis · 2026Article
- Regulated Cell Death in Calcium Oxalate Stone Disease: From Tubular Epithelial Injury to Inflammatory Amplification.Journal of inflammation research · 2026Review
- GGT1 protects against calcium oxalate crystal-induced renal tubular epithelial cell injury by targeting GCLC.Urolithiasis · 2025Article
- Bardoxolone methyl (Bard)-mediated strong suppression of calcium oxalate crystal formation in renal crystal recurrence model.Scientific reports · 2025Article
- Effects of micro-channel negative pressure sheath percutaneous nephrolithotomy versus extracorporeal shock wave lithotripsy for renal stones: risk factors for postoperative complications.American journal of translational research · 2025Article
- The Altered Proteomic Landscape in Renal Tubular Epithelial Cells under High Oxalate Stimulation.Biology · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Kidney stone is a common and highly recurrent disease in urology, and its pathogenesis is associated with various factors. However, its precise pathogenesis is still unknown. Ferroptosis describes a form of regulated cell death that is driven by unrestricted lipid peroxidation, which does not require the activation of caspase and can be suppressed by iron chelators, lipophilic antioxidants, inhibitors of lipid peroxidation, and depletion of polyunsaturated fatty acids. Recent studies have shown that ferroptosis plays a crucial role in kidney stone formation. An increasing number of studies have shown that calcium oxalate, urate, phosphate, and selenium deficiency induce ferroptosis and promote kidney stone formation through mechanisms such as oxidative stress, endoplasmic reticulum stress, and autophagy. We also offered a new direction for the downstream mechanism of ferroptosis in kidney stone formation based on the "death wave" phenomenon. We reviewed the emerging role of ferroptosis in kidney stone formation and provided new ideas for the future treatment and prevention of kidney stones.
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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.