ReviewInternational journal of molecular sciences2025
Reactive Oxygen Species (ROS) in Metabolic Disease-Don't Shoot the Metabolic Messenger.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Potential of Zinc-L-Selenomethionine to Improve the Health of Weaned Piglets and Its Antioxidant Stress Mechanism Through Modulation of PI3K/AKT and Nrf2/Keap1 Signaling Pathways.International journal of molecular sciences · 2026Article
- Review
- Advances in Coumarin Fluorescent Probes for Medical Diagnostics: A Review of Recent Developments.Biosensors · 2026Review
- Mechanistic insights and challenges in mitochondrial regulation of macrophage polarization and inflammatory responses.Frontiers in physiology · 2026Review
- Nicotinamide adenine dinucleotide phosphate oxidase 4 in lung disease: a review of its biology and therapeutic potential.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Medicinal Plants That Modulate Nitric Oxide Synthase Activity: Implications in Inflammation and Oxidative Stress.Drug design, development and therapy · 2026Review
- Mitochondrial medicine in obesity: a scoping review.Open medicine (Warsaw, Poland) · 2026Review
- Aging epicardial adipose tissue: a metabolic-endocrine network driving vascular calcification.Frontiers in endocrinology · 2026Review
- From Electron Imbalance to Network Collapse: Decoding the Redox Code of Ischemic Stroke for Biomarker-Guided Precision Neuroprotection.International journal of molecular sciences · 2025Review
- ROS homeostasis in cell fate, pathophysiology, and therapeutic interventions.Molecular biomedicine · 2025Review
- Article
- Antioxidants: powering the fight against fetal hypoxia.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Artificial Intelligence in Assessing Reproductive Aging: Role of Mitochondria, Oxidative Stress, and Telomere Biology.Diagnostics (Basel, Switzerland) · 2025Review
- Oxidative Stress-Driven Cellular Senescence: Mechanistic Crosstalk and Therapeutic Horizons.Antioxidants (Basel, Switzerland) · 2025Review
- Unraveling the complexities of diet induced obesity and glucolipid dysfunction in metabolic syndrome.Diabetology & metabolic syndrome · 2025Review
- Probiotics in Nanotechnology-Driven Wound Healing: From Mechanistic Insight to Clinical Promise.Pharmaceutics · 2025Review
- Biological Models of Oxidative Purine DNA Damage in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2025Review
- Cinnabar-induced hormesis inFrontiers in microbiology · 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) are widely considered key to pathogenesis in chronic metabolic disease. Consequently, much attention is rightly focused on minimising oxidative damage. However, for ROS production to be most effectively modulated, it is crucial to first appreciate that ROS do not solely function as pathological mediators. There are >90 gene products specifically evolved to generate, handle, and tightly buffer the cellular concentration of ROS. Therefore, it is likely that ROS plays a role as integral homeostatic signalling components and only become toxic in extremis. This review explores these commonly overlooked normal physiological functions, including how ROS are generated in response to environmental or hormonal stimuli, the mechanisms by which the signals are propagated and regulated, and how the cell effectively brings the signal to an end after an appropriate duration. In the course of this, several specific and better-characterised signalling mechanisms that rely upon ROS are explored, and the threshold at which ROS cross from beneficial signalling molecules to pathology mediators is discussed.
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.