ReviewGenes2017
The Mitochondrial Basis of Aging and Age-Related Disorders.
Review in Genes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 247 papers, 4 of them syntheses that pooled it.
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
247 citing papers in PubMed, 4 syntheses or guidelines pooled it, 402 citations in OpenAlex.
- Effects of Artificial Sweeteners on the Musculoskeletal System: A Systematic Review of Current Evidence.Nutrients · 2025Pooled it
- Effects of Intermittent Normobaric Hypoxia on Health-Related Outcomes in Healthy Older Adults: A Systematic Review.Sports medicine - open · 2023Pooled it
- Alcohol use disorder is associated with DNA methylation-based shortening of telomere length and regulated by TESPA1: implications for aging.Molecular psychiatry · 2022Pooled it
- Discovering the Potential Value of Coenzyme Q10 in Oxidative Stress: Enlightenment From a Synthesis of Clinical Evidence Based on Various Population.Frontiers in pharmacology · 2022Pooled it
- 4-Octyl Itaconate Attenuates Age-Induced Parotid Gland Dysfunction Through the Suppression of Fibrosis and Lipid Deposition by AMPKα/PPARα and the Inhibition of Oxidative Stress via the AMPKα/Nrf2 Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- A critical role for mitochondrial dynamics in cigarette smoke condensate-induced RPE senescence.Free radical biology & medicine · 2026Article
- Conserved signaling pathways and transcriptional regulators drive ovarian aging across species.Poultry science · 2026Article
- Palmitoylethanolamide and Luteolin in Brain Aging and Cognitive Decline: Biological Rationale and Current Evidence.Nutrients · 2026Review
- Astragalus membranaceus ameliorates endometrial aging and restores receptivity by enhancing mitochondrial function in stromal and epithelial cells.Protein & cell · 2026Article
- Metabolomic Profiling ofJournal of fungi (Basel, Switzerland) · 2026Article
- Ferroptosis-related stress during aging and its relevance to disease.GeroScience · 2026Review
- Review
- MSTO1 functions as a TRiC assembly factor linking cytosolic proteostasis to mitochondrial function.bioRxiv : the preprint server for biology · 2026Article
- Article
- Triphenylphosphonium compounds preferentially inhibit long-chain fatty acid oxidation in cardiac mitochondria.Research square · 2026Article
- Menaquinone-7 alleviates mitochondrial dysfunction and senescence in senile osteoporosis by targeting the PINK1-mediated mitophagy via PXR/ERK/CREB signaling pathway.Journal of pharmaceutical analysis · 2026Article
- Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026Review
- Oxidative Stress and Diminished Mitochondrial Proteostatic Reserve Are Linked to Enhanced mtUPR Initiation in Aged Mouse Muscle.Aging cell · 2026Article
- Beyond energy production: targeting mitochondrial biogenesis in aging and cancer with phytochemical intervention.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Article
187 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a natural phenomenon characterized by progressive decline in tissue and organ function leading to increased risk of disease and mortality. Among diverse factors that contribute to human aging, the mitochondrial dysfunction has emerged as one of the key hallmarks of aging process and is linked to the development of numerous age-related pathologies including metabolic syndrome, neurodegenerative disorders, cardiovascular diseases and cancer. Mitochondria are central in the regulation of energy and metabolic homeostasis, and harbor a complex quality control system that limits mitochondrial damage to ensure mitochondrial integrity and function. The intricate regulatory network that balances the generation of new and removal of damaged mitochondria forms the basis of aging and longevity. Here, I will review our current understanding on how mitochondrial functional decline contributes to aging, including the role of somatic mitochondrial DNA (mtDNA) mutations, reactive oxygen species (ROS), mitochondrial dynamics and quality control pathways. I will further discuss the emerging evidence on how dysregulated mitochondrial dynamics, mitochondrial biogenesis and turnover mechanisms contribute to the pathogenesis of age-related disorders. Strategies aimed to enhance mitochondrial function by targeting mitochondrial dynamics, quality control, and mitohormesis pathways might promote healthy aging, protect against age-related diseases, and mediate longevity.
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.