ReviewOxidative medicine and cellular longevity2021
Targeting the Mitochondrial Permeability Transition Pore to Prevent Age-Associated Cell Damage and Neurodegeneration.
Review in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.
- Emerging perspectives on mitochondrial dysfunctioning and inflammation in epileptogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Pooled it
- Mitochondrial Permeability Transition Regulators As Emerging Therapeutic Targets in Aging and Neurodegeneration: Recent Insights.Journal of molecular neuroscience : MN · 2026Review
- Silibinin promotes hepatocyte proliferation through PINK1/Parkin-mediated mitophagy to alleviate acetaminophen-induced liver injury.Clinical and experimental medicine · 2026Article
- Cardiac metabolic remodeling drives dicarbonyl stress-induced mitochondrial dysfunction in experimental heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2026Article
- Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026Review
- Fetal programming of the cardiac mitochondrial permeability transition pore in male offspring from hypoxic pregnancies.Redox biology · 2026Article
- Simvastatin-induced neuroprotective effect after brain injury is mediated by mitochondrial protection through modulation of the 18 kDa translocator protein.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- UNI-494 treatment improves measures of renal dysfunction and cardiac pathology in male rats receiving L-NAME and angiotensin II.Physiological reports · 2025Article
- Research progress in the regulatory mechanism of silent information regulator 1 in sepsis (Review).Molecular medicine reports · 2025Review
- Mitochondrial dysfunction mediated by ER-calcium dysregulation in neurons derived from Alzheimer's disease patients.Acta neuropathologica communications · 2025Article
- A Web of Challenges: The Therapeutic Struggle to Target NETs in Disease.International journal of molecular sciences · 2025Review
- Article
- Mechanisms of Mitochondria-Mediated Apoptosis DuringAnimals : an open access journal from MDPI · 2025Article
- A new perspective on protecting the blood-retinal barrier against injury in diabetic retinopathy: mitophagy.Frontiers in endocrinology · 2025Review
- Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- Neuroprotection against beta-amyloid toxicity by the novel estrogen receptor modulator STX requires convergent signaling pathways.Frontiers in molecular neuroscience · 2025Article
- 4-HNE-induced cellular dysfunction from lipid peroxidation: a potential therapeutic target in diabetic cardiomyopathy.Frontiers in cell and developmental biology · 2025Review
- Neuroprotective Effect of Resveratrol Propionate Esters on Apoptosis of SH-SY5Y Cells Induced by Hydrogen Peroxide.Biochemistry research international · 2025Article
- TRAP1 Improves Diabetic Retinopathy by Preserving Mitochondrial Function.Clinical ophthalmology (Auckland, N.Z.) · 2025Article
- Chitosan activates NLRP3 inflammasome and cGAS-STING to suppress cancer progression through hexokinase 2 dissociation and mitochondrial dysfunction.Theranostics · 2025Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
The aging process is associated with significant alterations in mitochondrial function. These changes in mitochondrial function are thought to involve increased production of reactive oxygen species (ROS), which over time contribute to cell death, senescence, tissue degeneration, and impaired tissue repair. The mitochondrial permeability transition pore (mPTP) is likely to play a critical role in these processes, as increased ROS activates mPTP opening, which further increases ROS production. Injury and inflammation are also thought to increase mPTP opening, and chronic, low-grade inflammation is a hallmark of aging. Nicotinamide adenine dinucleotide (NAD+) can suppress the frequency and duration of mPTP opening; however, NAD+ levels are known to decline with age, further stimulating mPTP opening and increasing ROS release. Research on neurodegenerative diseases, particularly on Parkinson's disease (PD) and Alzheimer's disease (AD), has uncovered significant findings regarding mPTP openings and aging. Parkinson's disease is associated with a reduction in mitochondrial complex I activity and increased oxidative damage of DNA, both of which are linked to mPTP opening and subsequent ROS release. Similarly, AD is associated with increased mPTP openings, as evidenced by amyloid-beta (A
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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 OpenQuestion graph.