ReviewAging cell2018
Mitochondria and aging: A role for the mitochondrial transition pore?
Review in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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
74 citing papers in PubMed, 142 citations in OpenAlex.
- Therapeutic potential of MitoQ, a mitochondria-targeted antioxidant, in age-related physiological dysfunction.GeroScience · 2026Review
- Review
- Genetic ablation of neuronal mitochondrial calcium uptake impedes Alzheimer's disease progression.The EMBO journal · 2026Article
- Mitochondrial drivers of stem cell aging and inflammaging.npj aging · 2026Review
- Ex vivo effects of low dose delayed release rapamycin on agonist-induced platelet aggregation, activation and procoagulant platelet phenotypes in domestic cats.Scientific reports · 2026Article
- Advances in Elucidating the Mitochondrial DNA Mechanisms Underlying Ozone-Induced Inflammation.Toxics · 2026Review
- Understanding cardiovascular aging as a disorder of mitochondrial network.The journal of cardiovascular aging · 2026Article
- Novel therapeutic strategies targeting mitochondrial quality control for metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2026Review
- Unraveling sex differences in age-related hippocampal decline: differential mitochondrial dysfunction, Lonp1-dependent mitochondrial proteostasis and mtROS production in aged C57BL/6 mice.Cell death & disease · 2025Article
- Article
- Oxidative phosphorylation and fatty acid oxidation in slow-aging mice.Free radical biology & medicine · 2024Review
- The effects of oxidative stress and intracellular calcium on mitochondrial permeability transition pore formation in equine spermatozoa.FASEB bioAdvances · 2024Article
- Cumulative Deleterious Effects of Tetrahydrocannabinoid (THC) and Ethanol on Mitochondrial Respiration and Reactive Oxygen Species Production Are Enhanced in Old Isolated Cardiac Mitochondria.International journal of molecular sciences · 2024Article
- Implications of endoplasmic reticulum stress and autophagy in aging and cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Dialogue between mitochondria and endoplasmic reticulum-potential therapeutic targets for age-related cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Mitochondria-sequestered Aβ renders synaptic mitochondria vulnerable in the elderly with a risk of Alzheimer disease.JCI insight · 2023Article
- Neuronal Senescence in the Aged Brain.Aging and disease · 2023Review
- Molecularly Targeted Fluorescent Sensors for Visualizing and Tracking Cellular Senescence.Biosensors · 2023Review
- Melatonin Alleviates Lipopolysaccharide-Induced Endometritis by Inhibiting the Activation of NLRP3 Inflammasome through Autophagy.Animals : an open access journal from MDPI · 2023Article
- Talk to Me-Interplay between Mitochondria and Microbiota in Aging.International journal of molecular sciences · 2023Review
14 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
3 authors at 1 institution in 1 country.
Funding
Abstract
The cellular mechanisms responsible for aging are poorly understood. Aging is considered as a degenerative process induced by the accumulation of cellular lesions leading progressively to organ dysfunction and death. The free radical theory of aging has long been considered the most relevant to explain the mechanisms of aging. As the mitochondrion is an important source of reactive oxygen species (ROS), this organelle is regarded as a key intracellular player in this process and a large amount of data supports the role of mitochondrial ROS production during aging. Thus, mitochondrial ROS, oxidative damage, aging, and aging-dependent diseases are strongly connected. However, other features of mitochondrial physiology and dysfunction have been recently implicated in the development of the aging process. Here, we examine the potential role of the mitochondrial permeability transition pore (mPTP) in normal aging and in aging-associated diseases.
Indexed as
Identifiers
What Socratic 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 Socratic graph.