ReviewThe Journal of clinical investigation2022
Mitochondrial dysfunction in cell senescence and aging.
Review in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 586 papers, 2 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
586 citing papers in PubMed, 2 syntheses or guidelines pooled it, 885 citations in OpenAlex.
- Antioxidant enzymes, oxidative stress, and physiological aging markers in Drosophila melanogaster (Diptera: Drosophilidae): a systematic review with translational perspectives.Journal of insect science (Online) · 2026Pooled it
- Histological and Genetic Markers of Cellular Senescence in Keratinocyte Cancers and Actinic Keratosis: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Ultrasound-activated piezoelectric patch enhances mitophagy and synergistic anti-inflammation to promote neurological repair after TBI.Bioactive materials · 2027Article
- Age-dependent mitochondrial toxicity in renal stem cells: A precise 3D silk matrix model.Genes & diseases · 2026Article
- Mitochondrial dysfunction and inflammaging: a mechanistic bridge between bioenergetic failure and senescence.GeroScience · 2026Review
- Mechanistic reprogramming of the mtDNA-cGAS-STING axis in cellular senescence: from mitochondrial homeostatic disruption to inflammatory and immune outcomes.Biogerontology · 2026Review
- Remodeling of mitochondrial dynamics by metabolic pathways couples to oncogenic growth inScience advances · 2026Article
- A biomimetic chondrocyte membrane-camouflaged tFNA nanoplatform for reprogramming the cartilage-synovium axis in osteoarthritis.Materials today. Bio · 2026Article
- A tumor microenvironment-responsive calcium overload nanoplatform inducing PANoptosis for enhanced cancer immunotherapy.Materials today. Bio · 2026Article
- Elamipretide Rejuvenates Oocyte Quality and Restores Female Fertility During Reproductive Aging.Aging cell · 2026Article
- Inhibiting Glutaminase Reverses Senescence-Associated Mitochondrial Dysfunction and Skeletal Muscle Decline.Aging cell · 2026Article
- Review
- Therapeutic potential of MitoQ, a mitochondria-targeted antioxidant, in age-related physiological dysfunction.GeroScience · 2026Review
- Persistent ZnAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Senescent Cell Heterogeneity: Tissue-Dependent Signatures and Age Dynamics Revealed by Human scRNA-Seq Data.International journal of molecular sciences · 2026Article
- Dual Roles of Autophagy in Endometrial Fibrosis and Its Implications in Age-Related Reproductive Dysfunction.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Replicative and Air Pollution-Induced Senescence: Telomere Dysfunction, Mitochondrial Stress, and Modulatory Effects of Astragaloside IV in Endothelial and Vascular Smooth Muscle Cells.Cardiovascular toxicology · 2026Article
- Mitochondrial homeodynamics in ageing: mechanisms, resilience, and interventions.Biogerontology · 2026Review
- SIRT1 in Senescence: Mitochondria and Immune Crosstalk.Biology · 2026Review
- Role of HMGB1 in Neuroinflammation.Molecular neurobiology · 2026Review
526 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondrial dysfunction and cell senescence are hallmarks of aging and are closely interconnected. Mitochondrial dysfunction, operationally defined as a decreased respiratory capacity per mitochondrion together with a decreased mitochondrial membrane potential, typically accompanied by increased production of oxygen free radicals, is a cause and a consequence of cellular senescence and figures prominently in multiple feedback loops that induce and maintain the senescent phenotype. Here, we summarize pathways that cause mitochondrial dysfunction in senescence and aging and discuss the major consequences of mitochondrial dysfunction and how these consequences contribute to senescence and aging. We also highlight the potential of senescence-associated mitochondrial dysfunction as an antiaging and antisenescence intervention target, proposing the combination of multiple interventions converging onto mitochondrial dysfunction as novel, potent senolytics.
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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.