ReviewMediators of inflammation2013
Mitochondrial dysfunction: a basic mechanism in inflammation-related non-communicable diseases and therapeutic opportunities.
Review in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 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
88 citing papers in PubMed, 154 citations in OpenAlex.
- Advanced Antioxidant Science is Reshaping the Battle Against Metabolic Syndrome: Next-Generation Approaches to Unlock Oxidative Stress Solutions.Indian journal of clinical biochemistry : IJCB · 2025Article
- The acute exercise response of peripheral blood mononuclear cells and their bioenergetic function in women with high and low systemic estradiol levels.Physiological reports · 2025Article
- From Obesity to Mitochondrial Dysfunction in Peripheral Tissues and in the Central Nervous System.Biomolecules · 2025Review
- Immunometabolic integration in therapeutic strategies for managing MASLD.Frontiers in pharmacology · 2025Review
- Nitrate-Nitrite-Nitric Oxide Pathway, Oxidative Stress, and Fertility Outcomes in Morbidly Obese Women Following Bariatric Surgery: A Systematic Review.Biomedicines · 2024Review
- Targeting Mitochondrial Dysfunction for the Prevention and Treatment of Metabolic Disease by Bioactive Food Components.Journal of lipid and atherosclerosis · 2024Review
- HTRA2/OMI-Mediated Mitochondrial Quality Control Alters Macrophage Polarization Affecting Systemic Chronic Inflammation.International journal of molecular sciences · 2024Review
- Oxidative Stress, Inflammation, and Mitochondrial Dysfunction: A Link between Obesity and Atrial Fibrillation.Antioxidants (Basel, Switzerland) · 2024Review
- The role of macrophage and adipocyte mitochondrial dysfunction in the pathogenesis of obesity.Frontiers in immunology · 2024Review
- Beneficial Effects of Capybara Oil Supplementation on Steatosis and Liver Apoptosis in Obese Mice.Journal of obesity · 2024Article
- Role of Fish Oil in Preventing Paternal Obesity and Improving Offspring Skeletal Muscle Health.Biomedicines · 2023Article
- Inflammation: the driver of poor outcomes among children with severe acute malnutrition?Nutrition reviews · 2023Review
- Article
- Visceral Adipose Tissue Bioenergetics Varies According to Individuals' Obesity Class.International journal of molecular sciences · 2023Article
- The mediating role of inflammaging between mitochondrial dysfunction and sarcopenia in aging: a review.American journal of clinical and experimental immunology · 2023Review
- Mitochondria as a therapeutic: a potential new frontier in driving the shift from tissue repair to regeneration.Regenerative biomaterials · 2023Review
- The Hepatic Mitochondrial Alterations Exacerbate Meta-Inflammation in Autism Spectrum Disorders.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- A preliminary model of football-related neural stress that integrates metabolomics with transcriptomics and virtual reality.iScience · 2022Article
- Construction of a mitochondrial dysfunction related signature of diagnosed model to obstructive sleep apnea.Frontiers in genetics · 2022Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is not necessarily a predisposing factor for disease. It is the handling of fat and/or excessive energy intake that encompasses the linkage of inflammation, oxidation, and metabolism to the deleterious effects associated with the continuous excess of food ingestion. The roles of cytokines and insulin resistance in excessive energy intake have been studied extensively. Tobacco use and obesity accompanied by an unhealthy diet and physical inactivity are the main factors that underlie noncommunicable diseases. The implication is that the management of energy or food intake, which is the main role of mitochondria, is involved in the most common diseases. In this study, we highlight the importance of mitochondrial dysfunction in the mutual relationships between causative conditions. Mitochondria are highly dynamic organelles that fuse and divide in response to environmental stimuli, developmental status, and energy requirements. These organelles act to supply the cell with ATP and to synthesise key molecules in the processes of inflammation, oxidation, and metabolism. Therefore, energy sensors and management effectors are determinants in the course and development of diseases. Regulating mitochondrial function may require a multifaceted approach that includes drugs and plant-derived phenolic compounds with antioxidant and anti-inflammatory activities that improve mitochondrial biogenesis and act to modulate the AMPK/mTOR pathway.
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.