ArticleInternational journal of biological sciences2025
Remote Ischemic Preconditioning Attenuates Mitochondrial Dysfunction and Ferroptosis of Tubular Epithelial Cells by Inhibiting NOX4-ROS Signaling in Acute Kidney Injury.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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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
19 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Impact of acute kidney injury in different ECMO modalities: a multicenter retrospective study on risk factors and mortality.Renal failure · 2026Article
- Article
- Ferroptosis: Newly Emerged Regulator for Human Disease.MedComm · 2026Review
- Role of NOX4 and GSH in Cadmium-Induced Renal Redox Homeostatic Dysregulation of Rats and APO Intervention Effect Study.Biological trace element research · 2026Article
- Clinical implications of ferroptosis in critical illness: a narrative review.Journal of intensive care · 2026Review
- Translational Barriers and Optimization Strategies for Remote Ischemic Conditioning to Enhance Stroke Cerebroprotection.Biomolecules · 2026Review
- Mitochondria in Renal Ischemia-Reperfusion Injury: From Mechanisms to Therapeutics.Biomedicines · 2026Review
- Effect of remote ischemic preconditioning on the risk of contrast-induced acute kidney injury in patients with coronary heart disease undergoing percutaneous coronary intervention.Frontiers in cardiovascular medicine · 2026Article
- Renoprotective mechanisms of bioconverted wild-simulated ginseng: mitigating oxidative stress, inflammation, and apoptosis to protect against ischemic renal injury via Nrf2/HO-1/NF-κB/caspase-3 signaling.Journal of ginseng research · 2026Article
- Cellular senescence of renal tubular epithelial cells in diabetic kidney disease: emerging mechanisms and targeted interventions.Frontiers in cell and developmental biology · 2026Review
- Mitochondrial dysfunction in immune cells during the perioperative period: mechanisms, emerging therapeutic strategies, and implications for multi-organ protection.Frontiers in immunology · 2026Review
- Mitoxyperilysis: Rethinking oxidative stress as a spatially constrained lethal signal.International journal of biological sciences · 2026Article
- Mitochondrial dysfunction in sepsis-associated acute kidney injury: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Association Between Iron Overload and the Risk of Ocular Hypertension, Primary Open-Angle Glaucoma, and Normal-Tension Glaucoma.Translational vision science & technology · 2025Article
- Review
- Article
- Genetic and Pharmacological Inhibition of NOX4 Protects Against Rhabdomyolysis-Induced Acute Kidney Injury Through Suppression of Endoplasmic Reticulum Stress.Antioxidants (Basel, Switzerland) · 2025Article
- Mitochondrial dysfunction and metabolic reprogramming in acute kidney injury: mechanisms, therapeutic advances, and clinical challenges.Frontiers in physiology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a worldwide clinical burden associated with high morbidity and mortality. Remote ischemic preconditioning (rIPC), a brief nonlethal ischemia and reperfusion (IR) in remote tissues or limbs, has been used in an attempt to protect against AKI, but its underlying signaling pathways has not been elucidated. In the present study, rIPC protected kidney function and pathological injury and mitigated NADPH oxidase 4 (NOX4) upregulation in different AKI models (cisplatin, LPS and IRI). Furthermore, rIPC significantly attenuated mitochondrial dysfunction and ameliorated tubular epithelial ferroptosis during AKI. Mechanistically, in wild-type AKI mice and TCMK-1 cells, rIPC effectively decreased kidney ROS production, preserved mitochondrial dynamics and mitophagy, and ameliorated tubular epithelial ferroptosis. Notably, these protective effects of rIPC were further enhanced by NOX4 knockout or silencing and mitigated by NOX4 overexpression. Our study showed that rIPC may attenuate mitochondrial dysfunction and ferroptosis in tubular epithelial cells in AKI by inhibiting NOX4-ROS signaling. NOX4 might be used as a biomarker for monitoring the biological effects of rIPC to optimize the rIPC protocol and facilitate future translational studies.
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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 Socratic graph.