SynthesisJournal of advanced research2023
Ferroptosis in acute kidney injury following crush syndrome: A novel target for treatment.
Synthesis in Journal of advanced research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- Kaempferol conjugated selenium nanoparticles mitigate kidney injury from rhabdomyolysis through antioxidant and anti-inflammatory actions via Nrf2/NF-κb pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The biphasic interactions between ferroptosis and oxidative stress: from molecular mechanisms to disease interventions.Molecular biology reports · 2026Review
- A natural remedy: Kidney-targeting nanoplatform for photoacoustic imaging-guided three-in-one theranostics of rhabdomyolysis-induced acute kidney injury.Materials today. Bio · 2026Article
- Knockdown of PTEN Inhibits Autophagy-Dependent Ferroptosis to Alleviate LPS-Induced Sepsis-Associated Acute Kidney Injury.Inflammation · 2026Article
- Deubiquitinase USP35 regulates MDM4 degradation to promote endothelial ferroptosis and renal injury progression.Cell death discovery · 2026Article
- Diagnostic performance of the lactate dehydrogenase-to-albumin ratio for early acute kidney injury in crush syndrome: a retrospective cohort study.BMC emergency medicine · 2026Article
- Biomarker-Based Diagnosis and Risk Stratification in Sepsis-Associated Acute Kidney Injury: From Molecular Mechanisms to Multimarker Panels.Diagnostics (Basel, Switzerland) · 2026Review
- Acute kidney injury over the past decade: from definition evolution to pathogenesis insights and innovative therapeutic strategies.Cellular and molecular life sciences : CMLS · 2026Review
- Morroniside inJournal of clinical biochemistry and nutrition · 2026Article
- PINK1 deacetylation by emodin-induced SIRT3 upregulation alleviates acute kidney injury by Inhibition of ferroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Curcumin pretreatment enhances the capacity of BMSC exosomes to attenuate renal ischemia-reperfusion injury by ferroptosis suppression via miR-16-5p/Smad3/Mb axis.Stem cell research & therapy · 2026Article
- Ferroptosis: A Double-Edged Sword in Cisplatin-Based Cancer Therapy and Acute Kidney Injury.Cancer management and research · 2026Review
- Ferroptosis-associated changes in transfusion-related acute lung injury in Sprague Dawley rats.Open medicine (Warsaw, Poland) · 2026Article
- Nicotinamide riboside alleviates sepsis-induced acute kidney injury by suppressing ferroptosis.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Isoquercitrin triggers the ferroptosis of ovarian cancer via SLC7A11-dependent manner to repress its tumorigenesis.Discover oncology · 2025Article
- Kidneys on the Frontline: Nephrologists Tackling the Wilds of Acute Kidney Injury in Trauma Patients-From Pathophysiology to Early Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- Ferroptosis in acinar cells of traumatic pancreatitis: implications for predictive, preventive, and personalized approaches in intra-abdominal infection management.The EPMA journal · 2025Article
- The efficiency of blood cell counts and inflammatory indices in prediction of need for acute kidney injury in patients with crush syndrome.BMC nephrology · 2025Article
- Urine pH is associated with the development of acute kidney injury in crush syndrome.Scientific reports · 2025Article
- Organellophagy regulates cell death:A potential therapeutic target for inflammatory diseases.Journal of advanced research · 2025Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCrush syndrome (CS) is a kind of traumatic and ischemic injury that seriously threatens life after prolonged compression. It is characterized by systemic inflammatory reaction, myoglobinuria, hyperkalemia and acute kidney injury (AKI). Especially AKI, it is the leading cause of death from CS. There are various cell death forms in AKI, among which ferroptosis is a typical form of cell death. However, the role of ferroptosis has not been fully revealed in CS-AKI. AIM OF REVIEW: This review aimed to summarize the evidence of ferroptosis in CS-AKI and its related molecular mechanism, discuss the therapeutic significance of ferroptosis in CS-AKI, and open up new ideas for the treatment of CS-AKI. KEY SCIENTIFIC CONCEPTS OF REVIEW: One of the main pathological manifestations of CS-AKI is renal tubular epithelial cell dysfunction and cell death, which has been attributed to massive deposition of myoglobin. Large amounts of myoglobin released from damaged muscle deposited in the renal tubules, impeding the normal renal tubules function and directly damaging the tubules with oxidative stress and elevated iron levels. Lipid peroxidation damage and iron overload are the distinguishing features of ferroptosis. Moreover, high levels of pro-inflammatory cytokines and damage-associated molecule pattern molecules (HMGB1, double-strand DNA, and macrophage extracellular trap) in renal tissue have been shown to promote ferroptosis. However, how ferroptosis occurs in CS-AKI and whether it can be a therapeutic target remains unclear. In our current work, we systematically reviewed the occurrence and underlying mechanism of ferroptosis in CS-AKI.
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