ReviewJournal of physiology and biochemistry2003
Mitochondrial control of neuron death and its role in neurodegenerative disorders.
Review in Journal of physiology and biochemistry, 2003. 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, 103 citations in OpenAlex.
- The therapeutic effect of nicotinamide riboside chloride on ameliorating alcohol-induced neuronal damage with a focus on mitochondrial unfolded protein response and mitophagy.Genes & diseases · 2026Article
- Short-term traffic-related gaseous pollutant exposure is associated with childhood bronchopneumonia hospitalization: a 10-year time-series study from Guangzhou, China.Frontiers in public health · 2026Article
- Sleep deprivation and risk for Parkinson's disease: evidence and therapeutic implications.Journal of neurology · 2025Review
- Understanding the Pathophysiology of Ischemic Stroke: The Basis of Current Therapies and Opportunity for New Ones.Biomolecules · 2024Review
- Mechanisms of Acupuncture in Improving Alzheimer's Disease Caused by Mitochondrial Damage.Chinese journal of integrative medicine · 2022Review
- Case report: Stereotactic body radiation therapy with 12 Gy for silencing refractory ventricular tachycardia.Frontiers in cardiovascular medicine · 2022Article
- Review
- Targeting the Mitochondrial Permeability Transition Pore to Prevent Age-Associated Cell Damage and Neurodegeneration.Oxidative medicine and cellular longevity · 2021Review
- Mitochondrial Degeneration and Autophagy Associated With Delayed Effects of Radiation in the Mouse Brain.Frontiers in aging neuroscience · 2019Article
- Transient Cerebral Ischemia Promotes Brain Mitochondrial Dysfunction and Exacerbates Cognitive Impairments in Young 5xFAD Mice.PloS one · 2015Article
- Risk of Amyotrophic Lateral Sclerosis in Patients With Diabetes: A Nationwide Population-Based Cohort Study.Journal of epidemiology · 2015Article
- Mitochondrial dysfunction in amyotrophic lateral sclerosis - a valid pharmacological target?British journal of pharmacology · 2014Review
- In vitro neuroprotective potential of four medicinal plants against rotenone-induced toxicity in SH-SY5Y neuroblastoma cells.BMC complementary and alternative medicine · 2013Article
- Article
- Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency.Brain research · 2012Article
- Mitochondrial dynamics and mitophagy in the 6-hydroxydopamine preclinical model of Parkinson's disease.Parkinson's disease · 2012Article
- Role of calcium and mitochondria in MeHg-mediated cytotoxicity.Journal of biomedicine & biotechnology · 2012Review
- Role of oxidative stress and the mitochondrial permeability transition in methylmercury cytotoxicity.Neurotoxicology · 2011Article
- Post-injury administration of the mitochondrial permeability transition pore inhibitor, NIM811, is neuroprotective and improves cognition after traumatic brain injury in rats.Journal of neurotrauma · 2011Article
- Cyclophilin D deficiency improves mitochondrial function and learning/memory in aging Alzheimer disease mouse model.Neurobiology of aging · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic or functional mitochondrial alterations can result in the initiation of cell death programs that are believed to contribute to cell death in diabetes, ageing and neurodegenerative disorders. Mitochondria are being considered the main link between cellular stress signals activated during acute and chronic nerve cell injury, and the execution of nerve cell death. This second function of mitochondria is regulated by several families of proteins that can trigger an increase in permeability of the outer and/or inner mitochondrial membrane. One example of this is the formation of the mitochondrial permeability transition pore (MPTP). This process can trigger the release of cell death-inducing factors from mitochondria, as well as a dissipation of the mitochondrial transmembrane potential, depletion of ATP, and increased free radical formation. Among the factors released from mitochondria are cytochrome c, the apoptosis inductor factor (AIF), and caspases. We review the role of the MPTP in diverse physiological and pathological processes, including neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis (ALS). The design of drugs that could interfere with the functions of the MPTP could allow novel therapeutic approaches for the treatment of acute and chronic nerve cell injury.
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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.