ArticleCell death & disease2021
Cofilin1 oxidation links oxidative distress to mitochondrial demise and neuronal cell death.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Mild Hypothermia Alleviates Ischemia and Reperfusion Injury by Activating PINK1/Parkin Mitophagy.Neurochemical research · 2026Article
- Cofilin 1-138 Promotes Mitochondrial Dysfunction and Synaptic Degeneration in Parkinson's Disease.Molecular neurobiology · 2026Article
- Mechanisms of actin-binding proteins in glycolysis-cytoskeleton coupling.Journal of translational medicine · 2026Review
- Cofilin-1 is a redox-sensitive guard of the NLRP3 inflammasome.Nature immunology · 2026Article
- Cofilin-1 Exacerbates Tau-Induced Mitochondrial Damage, Oxidative Stress, and Apoptosis in Alzheimer's Disease.Neurochemical research · 2026Article
- Novel mechanism of neuronal hypoxia response: HIF-1α/STOML2 mediated PINK1-dependent mitophagy activation against neuronal injury.Cell death discovery · 2026Article
- PANoptosis and mitochondrial regulatory mechanisms in cerebral ischemia-reperfusion injury.Frontiers in physiology · 2026Review
- Molecular mechanisms of excitotoxicity and their relevance to the pathogenesis of neurodegenerative diseases-an update.Acta pharmacologica Sinica · 2025Review
- N-terminal α-amino SUMOylation promotes phosphorylation-independent cofilin-1 translocation to the mitochondrial matrix and induces apoptosis.Nature communications · 2025Article
- Repurposing Cofilin-Targeting Compounds for Ischemic Stroke Through Cheminformatics and Network Pharmacology.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Piper Kadsura Extract and its Bioactive Components Attenuates AβNeurochemical research · 2025Article
- Cofilin(s) and Mitochondria: Function Beyond Actin Dynamics.International journal of molecular sciences · 2025Review
- ARHGAP26 deficiency drives the oocyte aneuploidy and early embryonic development failure.Cell death and differentiation · 2025Article
- Ellman's Assay on the Surface: Thiol Quantification of Human Cofilin-1 Protein through Surface Plasmon Resonance.Langmuir : the ACS journal of surfaces and colloids · 2024Article
- Drp1 depletion protects against ferroptotic cell death by preserving mitochondrial integrity and redox homeostasis.Cell death & disease · 2024Article
- Review
- α-Synuclein-mediated mitochondrial translocation of cofilin-1 leads to oxidative stress and cell apoptosis in PD.Frontiers in neuroscience · 2024Article
- New insights into the ferroptosis and immune infiltration in endometriosis: a bioinformatics-based analysis.Frontiers in immunology · 2024Article
- Evaluation of the differences in proteomics of high-quality bovine colostrum and low-quality bovine colostrum.Veterinary medicine and science · 2023Article
- The mechanism of ferroptosis and its related diseases.Molecular biomedicine · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Many cell death pathways, including apoptosis, regulated necrosis, and ferroptosis, are relevant for neuronal cell death and share common mechanisms such as the formation of reactive oxygen species (ROS) and mitochondrial damage. Here, we present the role of the actin-regulating protein cofilin1 in regulating mitochondrial pathways in oxidative neuronal death. Cofilin1 deletion in neuronal HT22 cells exerted increased mitochondrial resilience, assessed by quantification of mitochondrial ROS production, mitochondrial membrane potential, and ATP levels. Further, cofilin1-deficient cells met their energy demand through enhanced glycolysis, whereas control cells were metabolically impaired when challenged by ferroptosis. Further, cofilin1 was confirmed as a key player in glutamate-mediated excitotoxicity and associated mitochondrial damage in primary cortical neurons. Using isolated mitochondria and recombinant cofilin1, we provide a further link to toxicity-related mitochondrial impairment mediated by oxidized cofilin1. Our data revealed that the detrimental impact of cofilin1 on mitochondria depends on the oxidation of cysteine residues at positions 139 and 147. Overall, our findings show that cofilin1 acts as a redox sensor in oxidative cell death pathways of ferroptosis, and also promotes glutamate excitotoxicity. Protective effects by cofilin1 inhibition are particularly attributed to preserved mitochondrial integrity and function. Thus, interfering with the oxidation and pathological activation of cofilin1 may offer an effective therapeutic strategy in neurodegenerative diseases.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.