ArticleJCI insight2023
REST contributes to AKI-to-CKD transition through inducing ferroptosis in renal tubular epithelial cells.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 34 citations in OpenAlex.
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Article
- Layered double hydroxide nanocarriers loaded with butylphthalide attenuate the AKI-CKD transition by regulating mitophagy.Materials today. Bio · 2026Article
- Dynamic Regulation of Ferroptosis in a Neonatal Rat Model of Postnatal Hypoxia-Induced Acute Kidney Injury.Antioxidants (Basel, Switzerland) · 2026Article
- Interactions between the gut microbiome and ferroptosis in degenerative diseases: Novel mechanisms and potential therapeutic strategies.Acta pharmaceutica Sinica. B · 2026Review
- Transcriptomics, Proteomics and Network Pharmacology Reveal the Mechanisms of Cantharidin-Induced Kidney Injury in Rats.Current issues in molecular biology · 2026Article
- Clarifying the Robustness of the Cyp7b1/27-Hydroxycholesterol Axis in Ferroptosis Susceptibility within Proximal Straight Tubules in Ischemic Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2026Article
- Licochalcone A mitigates cisplatin-induced nephrotoxicity by inhibiting ferroptosis and mitochondrial dysfunction via the Nrf2/GPX4 axis.Frontiers in pharmacology · 2026Article
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
- March6 Protects Against Acute Kidney Injury by Suppressing Renal Tubular Epithelial Cell Ferroptosis Through the Destabilization of P53 and ACSL4 Proteins.Inflammation · 2025Article
- Sirtuin Family in Acute Kidney Injury: Insights into Cellular Mechanisms and Potential Targets for Treatment.Biomolecules · 2025Review
- NSD1-916aa encoded by CircNSD1 contributes to AKI-to-CKD transition through inducing ferroptosis in tubular epithelial cells.JCI insight · 2025Article
- The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis.Nature communications · 2025Article
- Caffeic acid phenethyl ester protects renal tubular epithelial cells against ferroptosis in diabetic kidney disease via restoring PINK1-mediated mitophagy.Molecular medicine (Cambridge, Mass.) · 2025Article
- Harnessing the power of nanoagents in acute kidney injury: A versatile platform for imaging and treatment.Coordination chemistry reviews · 2025Article
- HNF3α Targets Nckap1l and Promotes Renal Fibrosis Following Ischemia-Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- REST contributes to renal fibrosis through inducing mitochondrial energy metabolism imbalance in tubular epithelial cells.Cell communication and signaling : CCS · 2025Article
- Persistent subclinical renal injury in female rats following renal ischemia-reperfusion injury.Clinical science (London, England : 1979) · 2025Article
- Important molecular mechanisms in ferroptosis.Molecular and cellular biochemistry · 2025Review
- Fabry Disease Podocytes Reveal Ferroptosis as a Potential Regulator of Cell Pathology.Kidney international reports · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic-reperfusion injury (IRI) is a major pathogenic factor in acute kidney injury (AKI), which directly leads to the hypoxic injury of renal tubular epithelial cells (RTECs). Although emerging studies suggest repressor element 1-silencing transcription factor (REST) as a master regulator of gene repression under hypoxia, its role in AKI remains elusive. Here, we found that REST was upregulated in AKI patients, mice, and RTECs, which was positively associated with the degree of kidney injury, while renal tubule-specific knockout of Rest significantly alleviated AKI and its progression to chronic kidney disease (CKD). Subsequent mechanistic studies indicated that suppression of ferroptosis was responsible for REST-knockdown-induced amelioration of hypoxia-reoxygenation injury, during which process Cre-expressing adenovirus-mediated REST downregulation attenuated ferroptosis through upregulating glutamate-cysteine ligase modifier subunit (GCLM) in primary RTECs. Further, REST transcriptionally repressed GCLM expression via directly binding to its promoter region. In conclusion, our findings revealed the involvement of REST, a hypoxia regulatory factor, in AKI-to-CKD transition and identified the ferroptosis-inducing effect of REST, which may serve as a promising therapeutic target for ameliorating AKI and its progression to CKD.
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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.