ReviewAntioxidants & redox signaling2018
Mitochondrial Reactive Oxygen Species and Type 1 Diabetes.
Review in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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
48 citing papers in PubMed, 102 citations in OpenAlex.
- Metabolic switch: lymphocytes and the onset of T-cell-mediated autoimmunity.Cellular & molecular immunology · 2026Review
- Mitochondrial dysfunction in type 1 diabetes and its implications for pancreatic beta-cell survival and insulin secretion.Acta diabetologica · 2026Review
- Role of Antioxidants in Diseases and its Impact on Mitochondria with A Focus on Diabetes: An Overview.Current drug research reviews · 2026Review
- Bone marrow mesenchymal stem cells-derived exosomes protect against β-cell destruction models and kidney injury by suppressing ferroptosis.Scientific reports · 2025Article
- Molecular and Inflammatory Etiologies of β-Cell Dysfunction in Type 1 Diabetes.Physiology (Bethesda, Md.) · 2025Review
- Inter-Organelle Crosstalk in Oxidative Distress: A Unified TRPM2-NOX2 Mediated Vicious Cycle Involving CaAntioxidants (Basel, Switzerland) · 2025Review
- Type 1 Diabetes Mellitus and Vitamin D.International journal of molecular sciences · 2025Review
- Bioengineering Platelets Presenting PD-L1, Galectin-9 and BTLA to Ameliorate Type 1 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Could hypoxic conditioning augment the potential of mesenchymal stromal cell-derived extracellular vesicles as a treatment for type 1 diabetes?Stem cell research & therapy · 2025Review
- The protective roles of eugenol on type 1 diabetes mellitus through NRF2-mediated oxidative stress pathway.eLife · 2025Article
- Cai's herbal tea enhances mitochondrial autophagy of type 1 diabetic mellitus β cells through the AMPK/mTOR pathway and alleviates inflammatory response.Acta diabetologica · 2024Article
- Investigating the interplay between mitophagy and diabetic neuropathy: Uncovering the hidden secrets of the disease pathology.Pharmacological research · 2024Review
- Dysmetabolism of Peripheral Blood Monocytes in Type 1 Diabetes Mellitus.Bulletin of experimental biology and medicine · 2024Article
- Liver and Pancreatic Toxicity of Endocrine-Disruptive Chemicals: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2024Review
- Redox regulation of mNature cell biology · 2024Article
- Mitochondrial bioenergetics, metabolism, and beyond in pancreatic β-cells and diabetes.Frontiers in molecular biosciences · 2024Review
- Insufficient SIRT1 in macrophages promotes oxidative stress and inflammation during scarring.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Effects of multiple stressors on pancreatic human islets proteome reveal new insights into the pathways involved.Proteomics · 2023Article
- Pediatric Type 1 Diabetes: Mechanisms and Impact of Technologies on Comorbidities and Life Expectancy.International journal of molecular sciences · 2023Review
- Identifying Redox-Sensitive Cysteine Residues in Mitochondria.Antioxidants (Basel, Switzerland) · 2023Article
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 1 institution in 1 country.
Funding
Abstract
significanceThe complex etiology of type 1 diabetes (T1D) is the outcome of failures in regulating immunity in combination with beta cell perturbations. Mitochondrial dysfunction in beta cells and immune cells may be involved in T1D pathogenesis. Mitochondrial energy production is essential for the major task of beta cells (the secretion of insulin in response to glucose). Mitochondria are a major site of reactive oxygen species (ROS) production. Under immune attack, mitochondrial ROS (mtROS) participate in beta cell damage. Similarly, T cell fate during immune responses is tightly regulated by mitochondrial physiology, morphology, and metabolism. Production of mtROS is essential for signaling in antigen-specific T cell activation. Mitochondrial dysfunction in T cells has been noted as a feature of some human autoimmune diseases. Recent Advances: Preclinical and clinical studies indicate that mitochondrial dysfunction in beta cells sensitizes these cells to immune-mediated destruction via direct or indirect mechanisms. Sensitivity of beta cells to mtROS is associated with genetic T1D risk loci in human and the T1D-prone nonobese diabetic (NOD) mouse. Mitochondrial dysfunction and altered metabolism have also been observed in immune cells of NOD mice and patients with T1D. This immune cell mitochondrial dysfunction has been linked to deleterious functional changes. CRITICAL ISSUES: It remains unclear how mitochondria control T cell receptor signaling and downstream events, including calcium flux and activation of transcription factors during autoimmunity. FUTURE DIRECTIONS: Mechanistic studies are needed to investigate the mitochondrial pathways involved in autoimmunity, including T1D. These studies should seek to identify the role of mitochondria in regulating innate and adaptive immune cell activity and beta cell failure.
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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.