ArticleRedox biology2020
Paracrine regulation and improvement of β-cell function by thioredoxin.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- Thioredoxin protects against diabetic hearing loss by regulating TOMM22 mediated mitochondrial autophagy in hair cells and inhibiting microglial M1 polarization.Scientific reports · 2026Article
- Review
- Optimized Monothiol Thioredoxin Derivative (ORP100S) Protects In Vitro and In Vivo from Radiation and Chemotoxicity Without Promoting Tumor Proliferation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Selenium and Selenoproteins: Mechanisms, Health Functions, and Emerging Applications.Molecules (Basel, Switzerland) · 2025Review
- Redox Status as a Key Driver of Healthy Pancreatic Beta-Cells.Physiological research · 2024Review
- Hydrogen peroxide detoxification through the peroxiredoxin/thioredoxin antioxidant system: A look at the pancreatic β-cell oxidant defense.Vitamins and hormones · 2023Article
- 4-OI Protects MIN6 Cells from Oxidative Stress Injury by ReducingBiomolecules · 2022Article
- Role of Reactive Oxygen Species in Glucose Metabolism Disorder in Diabetic Pancreatic β-Cells.Biomolecules · 2022Review
- Changing Perspectives from Oxidative Stress to Redox Signaling-Extracellular Redox Control in Translational Medicine.Antioxidants (Basel, Switzerland) · 2022Review
- Selenium and Selenoproteins at the Intersection of Type 2 Diabetes and Thyroid Pathophysiology.Antioxidants (Basel, Switzerland) · 2022Review
- Antioxidant Therapy in Cancer: Rationale and Progress.Antioxidants (Basel, Switzerland) · 2022Review
- Loss and Recovery of Glutaredoxin 5 Is Inducible by Diet in a Murine Model of Diabesity and Mediated by Free Fatty Acids In Vitro.Antioxidants (Basel, Switzerland) · 2022Article
- Redox Homeostasis in Pancreatic β-Cells: From Development to Failure.Antioxidants (Basel, Switzerland) · 2021Review
- The Role of Thioredoxin/Peroxiredoxin in the β-Cell Defense Against Oxidative Damage.Frontiers in endocrinology · 2021Review
- Redox Enzymes of the Thioredoxin Family as Potential and Novel Markers in Pemphigus.Oxidative medicine and cellular longevity · 2021Article
- Early Predictors in the Onset of Type 2 Diabetes at Different Fasting Blood Glucose Levels.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The failure of insulin-producing β-cells is the underlying cause of hyperglycemia in diabetes mellitus. β-cell decay has been linked to hypoxia, chronic inflammation, and oxidative stress. Thioredoxin (Trx) proteins are major actors in redox signaling and essential for signal transduction and the cellular stress response. We have analyzed the cytosolic, mitochondrial, and extracellular Trx system proteins in hypoxic and cytokine-induced stress using β-cell culture, isolated pancreatic islets, and pancreatic islet transplantation modelling low oxygen supply. Protein levels of cytosolic Trx1 and Trx reductase (TrxR) 1 significantly decreased, while mitochondrial Trx2 and TrxR2 increased upon hypoxia and reoxygenation. Interestingly, Trx1 was secreted by β-cells during hypoxia. Moreover, murine and human pancreatic islet grafts released Trx1 upon glucose stimulation. Survival of transplanted islets was substantially impaired by the TrxR inhibitor auranofin. Since a release was prominent upon hypoxia, putative paracrine effects of Trx1 on β-cells were examined. In fact, exogenously added recombinant hTrx1 mitigated apoptosis and preserved glucose sensitivity in pancreatic islets subjected to hypoxia and inflammatory stimuli, dependent on its redox activity. Human subjects were studied, demonstrating a transient increase in extracellular Trx1 in serum after glucose challenge. This increase correlated with better pancreatic islet function. Moreover, hTrx1 inhibited the migration of primary murine macrophages. In conclusion, our study offers evidence for paracrine functions of extracellular Trx1 that improve the survival and function of pancreatic β-cells.
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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.