ReviewAging2012
Nutrient availability links mitochondria, apoptosis, and obesity.
Review in Aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed.
- Novel association of the obesity risk-allele near Fas Apoptotic Inhibitory Molecule 2 (FAIM2) gene with heart rate and study of its effects on myocardial infarction in diabetic participants of the PREDIMED trial.Cardiovascular diabetology · 2014Trial
- Multidimensional risk impact of obesity on breast cancer incidence, treatment, and prognosis.International journal of obesity (2005) · 2026Review
- From Lipids to Mitochondria: Shared Metabolic Alterations in Obesity and Alzheimer's Disease.Cells · 2026Review
- Repeatability and Variability of a High-Fat High-Fructose Diet-Induced Metabolic Syndrome Model in Young Adult Male Wistar Rats.Methods and protocols · 2026Article
- Mitochondrial medicine in obesity: a scoping review.Open medicine (Warsaw, Poland) · 2026Review
- Nutri-epigenetics of mitochondrial function and energy homeostasis in obesity.Genes & nutrition · 2025Review
- Transcriptomic profiling reveals neural-immune-stromal dysregulation and risk-associated gene signatures in advanced keratoconus.Scientific reports · 2025Article
- Association of the triglyceride-glucose index and its combination with obesity indices with cardio-renal-metabolic multimorbidity: two decades of follow-up in the Tehran Lipid and Glucose Study.Cardiovascular diabetology · 2025Article
- Evaluative performance of TyG-ABSI versus traditional indices in relation to cardiovascular disease and mortality: evidence from the U.S. NHANES.Cardiovascular diabetology · 2025Article
- Triglyceride glucose-weight-adjusted waist index as a cardiovascular mortality predictor: incremental value beyond the establishment of TyG-related indices.Cardiovascular diabetology · 2025Article
- Mitochondrial Dysfunction as a Biomarker of Illness State in Bipolar Disorder: A Critical Review.Brain sciences · 2024Review
- Deciphering the aging process through single-cell cytometric technologies.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2024Review
- Beneficial Effects of Capybara Oil Supplementation on Steatosis and Liver Apoptosis in Obese Mice.Journal of obesity · 2024Article
- Anterior Pituitary Transcriptomics Following a High-Fat Diet: Impact of Oxidative Stress on Cell Metabolism.Endocrinology · 2023Article
- The potential effect mechanism of high-fat and high-carbohydrate diet-induced obesity on anxiety and offspring of zebrafish.Eating and weight disorders : EWD · 2022Article
- Review
- Oxidative Stress, Plant Natural Antioxidants, and Obesity.International journal of molecular sciences · 2021Review
- Exenatide Attenuates Obesity-Induced Mitochondrial Dysfunction by Activating SIRT1 in Renal Tubular Cells.Frontiers in endocrinology · 2021Article
- Plant Extracts and Reactive Oxygen Species as Two Counteracting Agents with Anti- and Pro-Obesity Properties.International journal of molecular sciences · 2019Review
- Delayed Pulmonary Apoptosis of Diet-Induced Obesity Mice followingOxidative medicine and cellular longevity · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Mitochondria are the dominant source of the cellular energy requirements through oxidative phosphorylation, but they are also central players in apoptosis. Nutrient availability may have been the main evolutionary driving force behind these opposite mitochondrial functions: production of energy to sustain life and release of apoptotic proteins to trigger cell death. Here, we explore the link between nutrients, mitochondria and apoptosis with known and potential implications for age-related decline and metabolic syndromes.
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.