ReviewMolecular and cellular biochemistry2025
The role of ACSL4 in stroke: mechanisms and potential therapeutic target.
Review in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
17 citing papers in PubMed.
- ACSL4 in Alzheimer's disease: Pathogenetic mechanisms and potential therapeutic targets.Genes & diseases · 2026Review
- Interference with HMGB1 Inhibits Neuronal Ferroptosis Following Spinal Cord Injury through Targeting ACSL4.Neurochemical research · 2026Article
- Enriched Environment Suppresses Neuronal Ferroptosis Through SIRT1/AKT/GSK3β-Dependent Glycogen Metabolic Reprogramming After Cerebral Ischemia-Reperfusion.Antioxidants (Basel, Switzerland) · 2026Article
- Epigenetic Mechanisms Regulating Ferroptosis in Ischemic Stroke: From Pathogenesis to Therapeutic Targets.Cellular and molecular neurobiology · 2026Review
- ACSL4 Inhibition by AS-252424 Protects Visual Function by Suppressing RGC Ferroptosis After Retinal Ischemia Reperfusion Injury.Molecular neurobiology · 2026Article
- LC3 gene expression as a marker of autophagy in acute myeloid and lymphoblastic leukemia: a systematic review.Discover oncology · 2026Review
- Oxidative stress-regulatory role of miR-10b-5p in the diabetic human cornea revealed through integrated multi-omics analysis.Diabetologia · 2026Article
- Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.Frontiers in immunology · 2026Review
- ACSL4-Mediated Ferroptosis and its Biological Functions and Potential Therapeutic Significance in Liver Diseases.Current pharmaceutical design · 2026Review
- Prognostic Relevance of ACSL4 as a Serological Marker and Its Mediating Roles in Acute Supratentorial Intracerebral Hemorrhage: An Observational Analytical Study.International journal of general medicine · 2026Article
- Ferroptosis in Cerebral Ischemia/Reperfusion Injury: Mechanistic Drivers and Therapeutic Frontiers.Neuropsychiatric disease and treatment · 2026Review
- Long-chain acyl-CoA synthetases: biological functions, diseases and therapeutic targets.Molecular biomedicine · 2025Review
- Ferroptosis in Diabetic Cardiomyopathy and Atherosclerosis: Mechanisms and Clinical Prospects.International journal of molecular sciences · 2025Review
- Targeting Ferroptosis in Tumors: Novel Marine-Derived Compounds as Regulators of Lipid Peroxidation and GPX4 Signaling.Marine drugs · 2025Review
- Neuronal Injury after Ischemic Stroke: Mechanisms of Crosstalk Involving Necroptosis.Journal of molecular neuroscience : MN · 2025Review
- Targeting ferroptosis for neuroprotection: potential therapeutic avenues in neurodegenerative and neuropsychiatric diseases.Frontiers in physiology · 2025Review
- Modified Sanjia Powder ameliorates cognitive impairment and exerts neuroprotective effects in 5 × FAD mice: insights from quantitative proteomics.Frontiers in nutrition · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Stroke, as a neurological disorder with a poor overall prognosis, has long plagued the patients. Current stroke therapy lacks effective treatments. Ferroptosis has emerged as a prominent subject of discourse across various maladies in recent years. As an emerging therapeutic target, notwithstanding its initial identification in tumor cells associated with brain diseases, it has lately been recognized as a pivotal factor in the pathological progression of stroke. Acyl-CoA synthetase long-chain family member 4 (ACSL4) is a potential target and biomarker of catalytic unsaturated fatty acids mediating ferroptosis in stroke. Specifically, the upregulation of ACSL4 leads to heightened accumulation of lipid peroxidation products and reactive oxygen species (ROS), thereby exacerbating the progression of ferroptosis in neuronal cells. ACSL4 is present in various tissues and involved in multiple pathways of ferroptosis. At present, the pharmacological mechanisms of targeting ACSL4 to inhibit ferroptosis have been found in many drugs, but the molecular mechanisms of targeting ACSL4 are still in the exploratory stage. This paper introduces the physiopathological mechanism of ACSL4 and the current status of the research involved in ferroptosis crosstalk and epigenetics, and summarizes the application status of ACSL4 in modern pharmacology research, and discusses the potential application value of ACSL4 in the field of stroke.
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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.