ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
CHAC1 Mediates Endoplasmic Reticulum Stress-Dependent Ferroptosis in Calcium Oxalate Kidney Stone Formation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- The hippo-YAP1/TEAD1-SLC7A5 axis: uncovering a novel therapeutic target for oxalate-induced renal tubular ferroptosis.Redox report : communications in free radical research · 2026Article
- Integrative transcriptomic and single-cell analyses identify CD74 as a candidate regulator of ferroptosis in renal tubular cells during nephrolithiasis.Renal failure · 2026Article
- A mild photothermal-mediated neuroimmunomodulatory composite hydrogel reverses the inflammatory osteoclast precursor phenotype to promote osteoporotic bone defect healing.Bioactive materials · 2026Article
- SIRT5-Mediated Desuccinylation of ACAA2 Protects Against Calcium Oxalate-Induced Kidney Injury by Regulating Fatty Acid Oxidation to Suppress Mitochondrial Oxidative Injury and Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of key molecules and pathways in CaOx crystal-induced renal injury based on metabolomics and proteomics.International urology and nephrology · 2026Article
- Gypenosides Mitigate STEC-Induced Intestinal Injury Through Modulation of Ferroptosis Involving the ATF4-CHAC1-GPX4 Axis.Antioxidants (Basel, Switzerland) · 2026Article
- Phenylalanine primes renal tubular redox vulnerability and calcium oxalate crystal retention through a PPARδ-CPT1A fatty-acid oxidation axis.Redox biology · 2026Article
- Extracts ofPharmaceuticals (Basel, Switzerland) · 2026Article
- ATF4: Orchestrating Cellular Stress Adaptation, Metabolism, and Immune Regulation in Health and Disease.International journal of molecular sciences · 2026Review
- 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
- Review
- Supplemental exposure to polystyrene nanoplastics synergistically amplifies calcium oxalate crystal-induced injury to renal tubular epithelium, accelerating the formation of calcium oxalate kidney stones.Particle and fibre toxicology · 2026Article
- A novel ferroptosis- and endoplasmic reticulum stress-related gene signature for predicting prognosis, immune features and drug sensitivity in gastric cancer.Discover oncology · 2026Article
- H3K9 acetylation-dependent CHAC1 transcription in dihydroartemisinin-induced hepatic stellate cell ferroptosis.Chinese medical journal · 2026Article
- Organelle-specific regulation of ferroptosis.Biology direct · 2026Review
- Identification of Biomarker in Kidney Stone Disease by Integrating Transcriptomics and Olink Proteomics: A Case-Control Study.Journal of inflammation research · 2026Article
- Total flavonoids ofFrontiers in pharmacology · 2026Article
- Regulated Cell Death in Calcium Oxalate Stone Disease: From Tubular Epithelial Injury to Inflammatory Amplification.Journal of inflammation research · 2026Review
- Harnessing hollow Prussian blue nanozymes for efficient photothermal lithotripsy while protecting the kidneys from oxidative stress injury.Materials today. Bio · 2025Article
- Identification of Key Genes Associated with Endoplasmic Reticulum Stress in Calcium Oxalate Kidney Stones.Genes · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
The initiation of calcium oxalate (CaOx) kidney stone formation is highly likely to stem from injury to the renal tubular epithelial cells (RTECs) induced by stimulation from an aberrant urinary environment. CHAC1 plays a critical role in stress response mechanisms by regulating glutathione metabolism. Endoplasmic reticulum (ER) stress and ferroptosis are demonstrated to be involved in stone formation. This study attempted to elucidate the mechanism of ER stress-dependent ferroptosis and the role of CHAC1 in CaOx kidney stones. Here, regulating ER stress and CHAC1 expression are performed in in vivo and in vitro stone models. These findings indicated that 4-Phenylbutyric acid (4-PBA)treatment and CHAC1 deficiency alleviated the ferroptotic status, including restoring GSH content, suppressing Fe
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