ArticleThe EMBO journal2016
Mitochondria are required for pro-ageing features of the senescent phenotype.
Article in The EMBO journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 466 papers, 3 of them syntheses 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
466 citing papers in PubMed, 3 syntheses or guidelines pooled it, 754 citations in OpenAlex.
- Effects of exercise interventions on inflammatory biomarker levels in older adults with frailty and/or sarcopenia: a systematic review and meta-analysis.Frontiers in immunology · 2026Pooled it
- The biomedical application of inorganic metal nanoparticles in aging and aging-associated diseases.Journal of advanced research · 2025Pooled it
- Pooled it
- Activation of telomerase by TA-65 enhances immunity and reduces inflammation post myocardial infarction.GeroScience · 2023Trial
- The role of senescence in kidney ageing, injury and fibrosis.Nature reviews. Nephrology · 2026Review
- Ubiquitination-mediated degradation of NLRX1 drives metabolic vulnerability and accelerates intervertebral disc degeneration.Cell death and differentiation · 2026Article
- Quantitative proteomics reveals coordinated changes in the proteome during replicative senescence.Nature communications · 2026Article
- Metabolism licenses the senescence secretome.Cell research · 2026Article
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- A Six-Week Multimodal Functional Training Program Improves Physical Function and Modulates Redox Homeostasis in Older Women.Medical sciences (Basel, Switzerland) · 2026Article
- Mitochondrial Redox Failure Links Senescence-like Foam Cell Stress to Ferroptosis and Plaque Non-Resolution in Atherosclerosis.Antioxidants (Basel, Switzerland) · 2026Review
- Activation of pro-survival autophagy by a small molecule promoting p62 oligomerization.The Journal of biological chemistry · 2026Article
- Senescence Markers and Associated Transcriptomic Changes Are Expressed at Early Stages of Alzheimer's Neuropathology but Are Not Independently Related to Dementia.International journal of molecular sciences · 2026Article
- Article
- Aging-Related Changes in the Injury Response of the Peripheral Nervous System.Neuroscience bulletin · 2026Review
- Melatonin Preserves Mitochondrial Redox Balance in UVB-Exposed Human Keratinocytes.Antioxidants (Basel, Switzerland) · 2026Article
- Mitochondrial quality control in human ageing and longevity.Nature metabolism · 2026Review
- Metabolic Kinases as Regulators of Inter-Organelle Communication in Aging and Age-Related Diseases.Aging cell · 2026Review
- The role and potential therapeutic intervention of cellular senescence in intervertebral disc degeneration.Genes & diseases · 2026Review
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
406 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
28 authors at 7 institutions in 4 countries.
Funding
Abstract
Cell senescence is an important tumour suppressor mechanism and driver of ageing. Both functions are dependent on the development of the senescent phenotype, which involves an overproduction of pro-inflammatory and pro-oxidant signals. However, the exact mechanisms regulating these phenotypes remain poorly understood. Here, we show the critical role of mitochondria in cellular senescence. In multiple models of senescence, absence of mitochondria reduced a spectrum of senescence effectors and phenotypes while preserving ATP production via enhanced glycolysis. Global transcriptomic analysis by RNA sequencing revealed that a vast number of senescent-associated changes are dependent on mitochondria, particularly the pro-inflammatory phenotype. Mechanistically, we show that the ATM, Akt and mTORC1 phosphorylation cascade integrates signals from the DNA damage response (DDR) towards PGC-1β-dependent mitochondrial biogenesis, contributing to aROS-mediated activation of the DDR and cell cycle arrest. Finally, we demonstrate that the reduction in mitochondrial content in vivo, by either mTORC1 inhibition or PGC-1β deletion, prevents senescence in the ageing mouse liver. Our results suggest that mitochondria are a candidate target for interventions to reduce the deleterious impact of senescence in ageing tissues.
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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.