ReviewOncotarget2016
Reprogramming of energy metabolism as a driver of aging.
Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 81 citations in OpenAlex.
- Blood Cell Mitochondrial Respiration Increases With Age and Varies by Sex in Healthy Adults.Aging cell · 2026Article
- SS-31 improves the quality of maternally aged oocytes by ameliorating mitochondrial function and metabolism.Journal of ovarian research · 2026Article
- Age-related mitochondrial energy metabolism reprogramming occurs in granulosa cells during ovarian aging.Frontiers in endocrinology · 2026Observational
- Adjunctive EGb 761 treatment in patients with Parkinson's disease: a case series.Frontiers in aging neuroscience · 2026Article
- Autophagy: The convergence point of aging and cancer.Biochemistry and biophysics reports · 2025Review
- The Potential of Mitochondrial Therapeutics in the Treatment of Oxidative Stress and Inflammation in Aging.Molecular neurobiology · 2025Review
- Tracing mitochondrial marks of neuronal aging in iPSCs-derived neurons and directly converted neurons.Communications biology · 2025Article
- Integrative metabolomics and genomics reveal molecular signatures for type 2 diabetes and its cardiovascular complications.Cardiovascular diabetology · 2025Article
- Disrupted macrophage metabolic adaptation and function drive senescence-induced decline in vertebrate regeneration.Theranostics · 2025Article
- Article
- A metabolomic profile of biological aging in 250,341 individuals from the UK Biobank.Nature communications · 2024Article
- Efficacy of Human Recombinant Growth Hormone in Females of a Non-Obese Hyperglycemic Mouse Model after Birth with Low Birth Weight.International journal of molecular sciences · 2024Article
- Mitochondria, Autophagy and Inflammation: Interconnected in Aging.Cell biochemistry and biophysics · 2024Review
- Anecdotal Evidence Elucidates the Aging Process.Current aging science · 2024Article
- Carnitine acetyltransferase deficiency mediates mitochondrial dysfunction-induced cellular senescence in dermal fibroblasts.Aging cell · 2023Article
- The effect of metformin on influenza vaccine responses in nondiabetic older adults: a pilot trial.Immunity & ageing : I & A · 2023Article
- The bile acid TUDCA reduces age-related hyperinsulinemia in mice.Scientific reports · 2022Article
- Article
- A Non-Obese Hyperglycemic Mouse Model that Develops after Birth with Low Birthweight.Biomedicines · 2022Article
- Antiaging Effect of 4-Antioxidants (Basel, Switzerland) · 2022Article
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
Aging is characterized by progressive loss of cellular function and integrity. It has been thought to be driven by stochastic molecular damage. However, genetic and environmental maneuvers enhancing mitochondrial function or inhibiting glycolysis extend lifespan and promote healthy aging in many species. In post-fertile Caenorhabditis elegans, a progressive decline in phosphoenolpyruvate carboxykinase with age, and a reciprocal increase in pyruvate kinase shunt energy metabolism from oxidative metabolism to anaerobic glycolysis. This reduces the efficiency and total of energy generation. As a result, energy-dependent physical activity and other cellular functions decrease due to unmatched energy demand and supply. In return, decrease in physical activity accelerates this metabolic shift, forming a vicious cycle. This metabolic event is a determinant of aging, and is retarded by caloric restriction to counteract aging. In this review, we summarize these and other evidence supporting the idea that metabolic reprogramming is a driver of aging. We also suggest strategies to test this hypothesis.
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.