ReviewProtoplasma2014
Do we age because we have mitochondria?
Review in Protoplasma, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 24 citations in OpenAlex.
- Neuroprotective Effects of Tectoridin in HNeurochemical research · 2025Article
- Association of Apolipoprotein E4-related Microvascular Disease in the Alzheimer's Disease Hippocampal CA1 Stratum Radiatum.Neuroscience · 2023Article
- PKCε activator protects hippocampal microvascular disruption and memory defect in 3×Tg-Alzheimer's disease mice with cerebral microinfarcts.Frontiers in aging neuroscience · 2023Article
- HIV Promotes Neurocognitive Impairment by Damaging the Hippocampal Microvessels.Molecular neurobiology · 2022Article
- Hypoxia in Aging and Aging-Related Diseases: Mechanism and Therapeutic Strategies.International journal of molecular sciences · 2022Review
- Dysregulated Purine Metabolism Contributes to Age-Associated Lower Urinary Tract Dysfunctions.Advances in geriatric medicine and research · 2021Article
- Purine nucleoside phosphorylase inhibition ameliorates age-associated lower urinary tract dysfunctions.JCI insight · 2020Article
- Cerebral Mitochondrial Function and Cognitive Performance during Aging: A Longitudinal Study in NMRI Mice.Oxidative medicine and cellular longevity · 2020Article
- Article
- Hypoxia and aging.Experimental & molecular medicine · 2019Review
- MKK3 mediates inflammatory response through modulation of mitochondrial function.Free radical biology & medicine · 2015Article
- Parental age affects somatic mutation rates in the progeny of flowering plants.Plant physiology · 2015Article
- Methusalem's mystery.Protoplasma · 2014Article
- Systems Biology Profiling of AMD on the Basis of Gene Expression.Journal of ophthalmology · 2013Article
- Is there a role for oxidative stress and mitochondrial dysfunction in age-associated bladder disorders?Tzu chi medical journalReview
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
No grant is acknowledged in the PubMed record.
Abstract
The process of aging remains a great riddle. Production of reactive oxygen species (ROS) by mitochondria is an inevitable by-product of respiration, which has led to a hypothesis proposing the oxidative impairment of mitochondrial components (e.g., mtDNA, proteins, lipids) that initiates a vicious cycle of dysfunctional respiratory complexes producing more ROS, which again impairs function. This does not exclude other processes acting in parallel or targets for ROS action in other organelles than mitochondria. Given that aging is defined as the process leading to death, the role of mitochondria-based impairments in those organ systems responsible for human death (e.g., the cardiovascular system, cerebral dysfunction, and cancer) is described within the context of "garbage" accumulation and increasing insulin resistance, type 2 diabetes, and glycation of proteins. Mitochondrial mass, fusion, and fission are important factors in coping with impaired function. Both biogenesis of mitochondria and their degradation are important regulatory mechanisms stimulated by physical exercise and contribute to healthy aging. The hypothesis of mitochondria-related aging should be revised to account for the limitations of the degradative capacity of the lysosomal system. The processes involved in mitochondria-based impairments are very similar across a large range of organisms. Therefore, studies on model organisms from yeast, fungi, nematodes, flies to vertebrates, and from cells to organisms also add considerably to the understanding of human aging.
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.