ReviewCells2021
Targeting Mitochondrial Metabolism as a Strategy to Treat Senescence.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed.
- Cyclin-Dependent Kinases 4 and 6 Inhibitors: An Emerging Therapeutic Framework from Growth Suppression to Tumor Clearance.ACS pharmacology & translational science · 2026Review
- Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026Review
- Nuclear-Mitochondria Crosstalk in Senescent Adipose-Derived Stem Cells.Smart medicine · 2026Review
- Geroprotective applications of oleuropein and hydroxytyrosol through the hallmarks of ageing.GeroScience · 2026Review
- 2-Methoxystypandrone fromAntioxidants (Basel, Switzerland) · 2026Article
- Space radiation induces distinct senescent phenotypes: Implications for space travel.npj aging · 2025Article
- Cyclovirobuxine D ameliorates cardiomyocyte senescence in diabetic cardiomyopathy mice by enhancing mitochondrial function via sirtuin 3-ATP5O signal axis.Chinese medicine · 2025Article
- Efficacy of extracellular vesicles derived from mesenchymal stromal cells in regulating senescence:World journal of stem cells · 2025Article
- Exosomes from Adipose Tissue Mesenchymal Stem Cells, a Preliminary Study for In Vitro and In Vivo Application.Bioengineering (Basel, Switzerland) · 2025Article
- Elucidating the Role and Mechanism of Alpha-Enolase in Senescent Amelioration via Metabolic Reprogramming.Cell proliferation · 2025Article
- ε-Viniferin Rejuvenates Senescence viaPharmaceuticals (Basel, Switzerland) · 2025Article
- Oxidative Stress-Driven Cellular Senescence: Mechanistic Crosstalk and Therapeutic Horizons.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- Epigallocatechin Gallate inPharmaceuticals (Basel, Switzerland) · 2025Article
- Oxidative Stress and Redox Imbalance: Common Mechanisms in Cancer Stem Cells and Neurodegenerative Diseases.Cells · 2025Review
- Advances in biomarkers and diagnostic significance of organ aging.Fundamental research · 2025Review
- Sauchinone Ameliorates Senescence Through Reducing Mitochondrial ROS Production.Antioxidants (Basel, Switzerland) · 2025Article
- Article
- Klotho protects INS-1 pancreatic β-cells from senescence and enhances mitochondrial function.Frontiers in aging · 2025Article
- Synergistic ROS Reduction Through the Co-Inhibition of BRAF and p38 MAPK Ameliorates Senescence.Antioxidants (Basel, Switzerland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Mitochondria are one of organelles that undergo significant changes associated with senescence. An increase in mitochondrial size is observed in senescent cells, and this increase is ascribed to the accumulation of dysfunctional mitochondria that generate excessive reactive oxygen species (ROS). Such dysfunctional mitochondria are prime targets for ROS-induced damage, which leads to the deterioration of oxidative phosphorylation and increased dependence on glycolysis as an energy source. Based on findings indicating that senescent cells exhibit mitochondrial metabolic alterations, a strategy to induce mitochondrial metabolic reprogramming has been proposed to treat aging and age-related diseases. In this review, we discuss senescence-related mitochondrial changes and consequent mitochondrial metabolic alterations. We assess the significance of mitochondrial metabolic reprogramming for senescence regulation and propose the appropriate control of mitochondrial metabolism to ameliorate senescence. Learning how to regulate mitochondrial metabolism will provide knowledge for the control of aging and age-related pathologies. Further research focusing on mitochondrial metabolic reprogramming will be an important guide for the development of anti-aging therapies, and will provide novel strategies for anti-aging interventions.
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.