ReviewAntioxidants & redox signaling2013
Interacting with thioredoxin-1--disease or no disease?
Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 41 citations in OpenAlex.
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- Mechanisms of Protection Against Oxidative Stress During Hibernation.International journal of molecular sciences · 2026Review
- TXNIP regulates the proliferation of scar fibroblasts through oxidative stress.European journal of medical research · 2025Article
- Changing the gravity vector direction by inverted culture enhances radiation-induced cell damage.Biochemistry and biophysics reports · 2024Article
- Disulfide stress and its role in cardiovascular diseases.Redox biology · 2024Review
- Role of thioredoxin in chronic obstructive pulmonary disease (COPD): a promising future target.Respiratory research · 2023Review
- Thioredoxin-1 promotes the restoration of alveolar bone in periodontitis with diabetes.iScience · 2023Article
- Caffeine Inhibits Oxidative Stress- and Low Dose Endotoxemia-Induced Senescence-Role of Thioredoxin-1.Antioxidants (Basel, Switzerland) · 2023Article
- Thioredoxin-1 Is a Target to Attenuate Alzheimer-Like Pathology in Diabetic Encephalopathy by Alleviating Endoplasmic Reticulum Stress and Oxidative Stress.Frontiers in physiology · 2021Article
- Curcumin Ameliorates Heat-Induced Injury through NADPH Oxidase-Dependent Redox Signaling and Mitochondrial Preservation in C2C12 Myoblasts and Mouse Skeletal Muscle.The Journal of nutrition · 2020Article
- STVNa Attenuates Isoproterenol-Induced Cardiac Hypertrophy Response through the HDAC4 and Prdx2/ROS/Trx1 Pathways.International journal of molecular sciences · 2020Article
- A Cross-Sectional Study of Endogenous Antioxidants and Patterns of Dental Visits of Periodontitis Patients.International journal of environmental research and public health · 2019Article
- Molecular Mechanisms of Glucose Fluctuations on Diabetic Complications.Frontiers in endocrinology · 2019Review
- Interplay between Trx-1 and S100P promotes colorectal cancer cell epithelial-mesenchymal transition by up-regulating S100A4 through AKT activation.Journal of cellular and molecular medicine · 2018Article
- Nuclear Factor (Erythroid-Derived 2)-Like 2 and Thioredoxin-1 in Atherosclerosis and Ischemia/Reperfusion Injury in the Heart.Antioxidants & redox signaling · 2017Review
- Redox regulation of FoxO transcription factors.Redox biology · 2015Review
- Diabetic Cardiovascular Disease Induced by Oxidative Stress.International journal of molecular sciences · 2015Review
- Foxp1 Regulates the Proliferation of Hair Follicle Stem Cells in Response to Oxidative Stress during Hair Cycling.PloS one · 2015Article
- Aggregate-prone R120GCRYAB triggers multifaceted modifications of the thioredoxin system.Antioxidants & redox signaling · 2014Article
- Redox control of human mitochondrial outer membrane protein MitoNEET [2Fe-2S] clusters by biological thiols and hydrogen peroxide.The Journal of biological chemistry · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
significanceMany cardiovascular disorders are accompanied by a deregulated cellular redox balance resulting in elevated levels of intracellular reactive oxygen species (ROS). One major antioxidative cellular molecule is thioredoxin-1 (Trx-1). Its indispensability is demonstrated by the embryonic lethality of Trx-1 deficient mice. Trx-1 is ubiquitously expressed in cells and has numerous, diverse functions. It not only reduces oxidized proteins or, together with peroxiredoxins, detoxifies H(2)O(2), but also binds to several proteins and thereby regulates their functions. The interaction partners of Trx-1 differ depending on its localization in the cytosol or in the nucleus. RECENT ADVANCES/CRITICAL ISSUES: Over the past decade it has become clear that Trx-1 is not only critical for tumor functions, which has resulted in therapeutic approaches targeting this protein, but also essential for proper functions of the vasculature and the heart. Changes in post-translational modifications of Trx-1 or in its interactions with other proteins can lead to a switch from a physiologic state of cells and organs to diverse pathologies. This review provides insights into the role of Trx-1 in different physiological situations and cardiac hypertrophy, ischemia reperfusion injury, heart failure, atherosclerosis, and diabetes mellitus type 2, underscoring the central role of Trx-1 in cardiovascular health and disease. FUTURE DIRECTIONS: Thus, the manipulation of Trx-1 activity in the heart and/or vasculature, for example, by small molecules, seems to be a promising therapeutic option in cardiovascular diseases, as general anti-oxidant treatments would not take into account interactions of Trx-1 with other proteins and also eliminate vital ROS.
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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.