ReviewAging cell2024
Interactions between mitochondrial dysfunction and other hallmarks of aging: Paving a path toward interventions that promote healthy old age.
Review in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 41 citations in OpenAlex.
- Lactic Acid Bacteria-Fermented Natural Products: Mechanisms and Evidence for Ageing- and Stem-Cell-Related Outcomes.Foods (Basel, Switzerland) · 2026Review
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- Precision Nutraceuticals and Biomarkers of Healthy Aging: A Scoping Review of Human Studies on Nutrigenomic-Based Interventions.Medical sciences (Basel, Switzerland) · 2026Article
- Duration of Caloric Restriction Modulates Brain Redox Adaptation and Frailty During Aging.International journal of molecular sciences · 2026Article
- Article
- Progressive Metabolic Dysregulation from Prediabetes to Diabetes Revealed by Untargeted Metabolomics.International journal of molecular sciences · 2026Article
- Mitochondrial Dysfunction in Circulating Blood Cells and Biological Aging: A Review of Mechanisms and Evidence.Biomolecules · 2026Review
- Tuning the Fire: Context-Dependent Mitochondrial ROS Signaling, Mitohormesis, and Redox-Modulating Interventions.Biomolecules · 2026Review
- Interactions between rare variants in DNA repair genes and cardiometabolic risk explain more variability in cognitive function.GeroScience · 2026Article
- Treatment of age-related decreases in GTP levels restores endocytosis and autophagy.GeroScience · 2026Article
- Interplay Between Autophagy, Cellular Senescence, and Brain Aging: Neuroprotective Implications of Intermittent Fasting.Cellular and molecular neurobiology · 2026Review
- Article
- TDP-43-driven alternative splicing of UQCRC2 modulates mitochondrial bioenergetics.Biology direct · 2026Article
- Histone methyltransferase SET-18/SMYD2-mediated activation of NADase TIR-1d/SARM1 increases mtROS to promote aging.iScience · 2026Article
- Nanoscale Delivery of MicroRNAs via Extracellular Vesicles: Mechanisms Potential in Modulating Cellular Senescence.International journal of nanomedicine · 2026Review
- Nanoparticle-Based Tools to Study Hallmarks of Aging at the Molecular Level.International journal of nanomedicine · 2026Review
- Balanced polyunsaturated fatty acids diet prevents the D-galactose-induced neuroinflammation and cognitive impairments.Neuroscience applied · 2026Article
- Proteomics of aging: biomarkers for physiological systems and diseases.Frontiers in aging · 2026Review
- Mitochondrial haplogroups, but not heteroplasmy, are associated with midlife cognitive function.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Serum methylmalonic acid levels predict multisite bone mineral density decline in patients with suspected mitochondrial dysfunction.Journal of orthopaedic surgery and research · 2025Article
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 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current research on human aging has largely been guided by the milestone paper "hallmarks of aging," which were first proposed in the seminal 2013 paper by Lopez-Otin et al. Most studies have focused on one aging hallmark at a time, asking whether the underlying molecular perturbations are sufficient to drive the aging process and its associated phenotypes. More recently, researchers have begun to investigate whether aging phenotypes are driven by concurrent perturbations in molecular pathways linked to not one but to multiple hallmarks of aging and whether they present different patterns in organs and systems over time. Indeed, preliminary results suggest that more complex interactions between aging hallmarks must be considered and addressed, if we are to develop interventions that successfully promote healthy aging and/or delay aging-associated dysfunction and diseases. Here, we summarize some of the latest work and views on the interplay between hallmarks of aging, with a specific focus on mitochondrial dysfunction. Indeed, this represents a significant example of the complex crosstalk between hallmarks of aging and of the effects that an intervention targeted to a specific hallmark may have on the others. A better knowledge of these interconnections, of their cause-effect relationships, of their spatial and temporal sequence, will be very beneficial for the whole aging research field and for the identification of effective interventions in promoting healthy old age.
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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 Socratic graph.