ReviewNeurochemistry international2013
AIF, reactive oxygen species, and neurodegeneration: a "complex" problem.
Review in Neurochemistry international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 57 citations in OpenAlex.
- CRABS-ROC, A respirometry protocol for overcoming substrate limitations, reveals excess brain mitochondrial Complex I capacity.Free radical biology & medicine · 2025Article
- Hypoxia-ischemia and sexual dimorphism: modeling mitochondrial dysfunction using brain organoids.Cell & bioscience · 2025Review
- Exploring the role of parthanatos in CNS injury: Molecular insights and therapeutic approaches.Journal of advanced research · 2025Review
- NovelNeurology. Genetics · 2024Article
- Apoptosis-Inducing Factor 2 (AIF-2) Mediates a Caspase-Independent Apoptotic Pathway in the Tropical Sea Cucumber (International journal of molecular sciences · 2022Article
- Emerging role of PARP-1 and PARthanatos in ischemic stroke.Journal of neurochemistry · 2022Review
- New insights into targeting mitochondria in ischemic injury.Apoptosis : an international journal on programmed cell death · 2021Review
- Mechanism of Zinc Excitotoxicity: A Focus on AMPK.Frontiers in neuroscience · 2020Review
- Alternative splicing in human cancer cells is modulated by the amiloride derivative 3,5-diamino-6-chloro-N-(N-(2,6-dichlorobenzoyl)carbamimidoyl)pyrazine-2-carboxide.Molecular oncology · 2019Article
- Mitochondria as Potential Targets and Initiators of the Blue Light Hazard to the Retina.Oxidative medicine and cellular longevity · 2019Review
- Rapamycin treatment increases hippocampal cell viability in an mTOR-independent manner during exposure to hypoxia mimetic, cobalt chloride.BMC neuroscience · 2018Article
- Up-regulation of GluN2A-containing NMDA receptor protects cultured cortical neuron cells from oxidative stress.Heliyon · 2018Article
- A disease-associated Aifm1 variant induces severe myopathy in knockin mice.Molecular metabolism · 2018Article
- Depletion of the Receptor-Interacting Protein Kinase 3 (RIP3) Decreases Photoreceptor Cell Death During the Early Stages of Ocular Murine Cytomegalovirus Infection.Investigative ophthalmology & visual science · 2018Article
- Neuronal Cell Death.Physiological reviews · 2018Review
- Mitochondrial function in hypoxic ischemic injury and influence of aging.Progress in neurobiology · 2017Review
- Anti-Oxidative Stress Activity Is Essential for Amanita caesarea Mediated Neuroprotection on Glutamate-Induced Apoptotic HT22 Cells and an Alzheimer's Disease Mouse Model.International journal of molecular sciences · 2017Article
- Structural and biochemical insights of CypA and AIF interaction.Scientific reports · 2017Article
- Review
- Blue Light Action on Mitochondria Leads to Cell Death by Necroptosis.Neurochemical research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Apoptosis-inducing factor (AIF) is a flavin-binding mitochondrial intermembrane space protein that is implicated in diverse but intertwined processes that include maintenance of electron transport chain function, reactive oxygen species regulation, cell death, and neurodegeneration. In acute brain injury, AIF acquires a pro-death role upon translocation from the mitochondria to the nucleus, where it initiates chromatin condensation and large-scale DNA fragmentation. Although harlequin mice exhibiting an 80-90% global reduction in AIF protein are resistant to numerous forms of acute brain injury, they paradoxically undergo slow, progressive neurodegeneration beginning at three months of age. Brain deterioration, accompanied by markers of oxidative stress, is most pronounced in the cerebellum and retina, although it also occurs in the cortex, striatum, and thalamus. Loss of an AIF pro-survival function linked to assembly or stabilization of electron transport chain complex I underlies chronic neurodegeneration. To date, most studies of neurodegeneration have failed to adequately separate the relative importance of the mitochondrial and nuclear functions of AIF in determining the extent of injury, or whether oxidative stress plays a causative role. This review explores the complicated relationship among AIF, complex I, and the regulation of mitochondrial reactive oxygen species levels. It also discusses the controversial role of complex I deficiency in Parkinson's disease, and what can be learned from the AIF- and complex I-depleted harlequin mouse.
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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.