ReviewJournal of radiation research2018
Potential relationship between the biological effects of low-dose irradiation and mitochondrial ROS production.
Review in Journal of radiation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
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
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.
- Effect of curcumin intervention on radiation-induced injury: a GRADE-based systematic review and meta-analysis.BMC cancer · 2026Pooled it
- Hedgehog/GLI Signaling at the Interface of Sterol Metabolism, Mitochondrial ROS Signaling and Cellular Plasticity.Antioxidants (Basel, Switzerland) · 2026Review
- A Mitochondria-Targeted Nitroxide Radical Mitigates Radiation-Induced Liver Injury by Attenuating Oxidative Stress and Preserving Mitochondrial Function.Antioxidants (Basel, Switzerland) · 2026Article
- Nonlinear Redox-Immune Coupling Under Low-Dose-Rate Radiation: A Compartment-Specific Framework for Biological Responses-A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- From Exposure to Effect: Genetic and Epigenetic Biomarker-Guided Risk Assessment in Cardiac Imaging.International journal of molecular sciences · 2026Review
- Distinct DNA hydroxymethylation landscape and mitochondrial DNA rearrangement signatures induced by single- and multi-fraction alpha particle radiation in lung fibroblasts.Environmental epigenetics · 2026Article
- Low-Dose radiation risk in medicine: a look at risk models, challenges, and future prospects.Zeitschrift fur medizinische Physik · 2025Review
- Targeting the redox-programmed cell death axis in breast cancer: from molecular mechanisms to therapeutic resistance.Cell death discovery · 2025Review
- Gas Plasma Combination Therapies-Promises from Preclinical Oncology Research.Antioxidants (Basel, Switzerland) · 2025Review
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- Lyophilized apoptotic vesicles restore DNA damage and mitochondria dysfunction to ameliorate radiation enteritis.Journal of nanobiotechnology · 2025Article
- Mechanisms Underlying Radioresistance and Reversal Strategies in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2025Review
- Glutathione-associated redox regulation alleviates radio-resistance of canine cancer stem-like cells with low proteasome activity.Scientific reports · 2025Article
- Enhancing radiation-induced reactive oxygen species generation through mitochondrial transplantation in human glioblastoma.Scientific reports · 2025Article
- Article
- A Landscape of Cancer Initiation and Cancer Stem Cells.Cancers · 2025Article
- Navigating oxidative stress in oral bone regeneration: mechanisms and reactive oxygen species-regulating biomaterial strategies.Regenerative biomaterials · 2025Review
- Radioprotection redefined: drug discovery at the intersection of tardigrade biology and translational pharmacology.Frontiers in pharmacology · 2025Article
- Dual role of autophagy in bone metastasis: mechanistic insights and therapeutic targeting.American journal of clinical and experimental urology · 2025Review
- Role of oxidative stress in post-burn wound healing.Burns & trauma · 2025Review
26 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to ionizing radiation (IR) induces various types of DNA damage, of which DNA double-strand breaks are the most severe, leading to genomic instability, tumorigenesis, and cell death. Hence, cells have developed DNA damage responses and repair mechanisms. IR also causes the accumulation of endogenous reactive oxidative species (ROS) in the irradiated cells. Upon exposure to low-dose irradiation, the IR-induced biological effects mediated by ROS were relatively more significant than those mediated by DNA damage. Accumulating evidence suggests that such increase in endogenous ROS is related with mitochondria change in irradiated cells. Thus, in this review we focused on the mechanism of mitochondrial ROS production and its relationship to the biological effects of IR. Exposure of mammalian cells to IR stimulates an increase in the production of endogenous ROS by mitochondria, which potentially leads to mitochondrial dysfunction. Since the remains of damaged mitochondria could generate or leak more ROS inside the cell, the damaged mitochondria are removed by mitophagy. The disruption of this pathway, involved in maintaining mitochondrial integrity, could lead to several disorders (such as neurodegeneration) and aging. Thus, further investigation needs to be performed in order to understand the relationship between the biological effects of low-dose IR and mitochondrial integrity.
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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.