ReviewNeurochemistry international2007
The mitochondrial permeability transition in neurologic disease.
Review in Neurochemistry international, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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
81 citing papers in PubMed, 165 citations in OpenAlex.
- Bioequivalence and tolerability assessment of a novel intravenous ciclosporin lipid emulsion compared to branded ciclosporin in Cremophor ® EL.Clinical drug investigation · 2013Trial
- Mitochondrial calcium and ROS: present understanding and future directions.Mitochondrion · 2026Article
- NETs drive CD4⁺ T cell dysfunction in sepsis via mitochondrial ROS and impaired calcium signalling.Molecular medicine (Cambridge, Mass.) · 2026Article
- Evaluating the mechanisms and therapeutic potential of ZnO nanoparticles as selective anticancer agents for lung malignancies.Discover nano · 2026Review
- Involvement of SIRT3 downstream targets ANT1, VDAC, CYPD, and Drp1 in a rat model of hepatic encephalopathy: Therapeutic role of thymoquinone.Iranian journal of basic medical sciences · 2026Article
- Intravenously injected poly(amino acid) nanoformulation relieves spinal cord injury through synergistical modulation of microenvironments.Materials today. Bio · 2025Article
- Brain proteome changes after intracerebral hemorrhage in aged male and female mice.Neurobiology of disease · 2025Article
- Beyond Fluid Therapy: The Role of Vitamin C, Steroids, and Thiamine in Sepsis Management.Cureus · 2025Review
- Modulation of brain energy metabolism in hepatic encephalopathy: impact of glucose metabolic dysfunction.Metabolic brain disease · 2024Review
- Mitochondrial dysfunction in sepsis: mechanisms and therapeutic perspectives.Critical care (London, England) · 2024Review
- MCU-independent CaScientific reports · 2024Article
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- ANT-dependent MPTP underlies necrotic myofiber death in muscular dystrophy.Science advances · 2023Article
- IF1 ablation prevents ATP synthase oligomerization, enhances mitochondrial ATP turnover and promotes an adenosine-mediated pro-inflammatory phenotype.Cell death & disease · 2023Article
- Acai Berry (Life (Basel, Switzerland) · 2023Article
- Emerging Promise of Therapeutic Approaches Targeting Mitochondria in Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- Remodeling of Liver and Plasma Lipidomes in Mice Lacking Cyclophilin D.International journal of molecular sciences · 2022Article
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Traumatic Brain Injury and Gut Brain Axis: The Disruption of an Alliance.Reviews on recent clinical trials · 2022Review
- Enhancement ofMolecules (Basel, Switzerland) · 2021Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria, being the principal source of cellular energy, are vital for cell life. Yet, ironically, they are also major mediators of cell death, either by necrosis or apoptosis. One means by which these adverse effects occur is through the mitochondrial permeability transition (mPT) whereby the inner mitochondrial membrane suddenly becomes excessively permeable to ions and other solutes, resulting in a collapse of the inner membrane potential, ultimately leading to energy failure and cell necrosis. The mPT may also bring about the release of various factors known to cause apoptotic cell death. The principal factors leading to the mPT are elevated levels of intracellular Ca2+ and oxidative stress. Characteristically, the mPT is inhibited by cyclosporin A. This article will briefly discuss the concept of the mPT, its molecular composition, its inducers and regulators, agents that influence its activity and describe the consequences of its induction. Lastly, we will review its potential contribution to acute neurological disorders, including ischemia, trauma, and toxic-metabolic conditions, as well as its role in chronic neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis.
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.