ReviewFree radical biology & medicine2017
Modulation of signaling mechanisms in the heart by thioredoxin 1.
Review in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 65 citations in OpenAlex.
- NADPH-depletion micelles sensitizing apoptotic and ferroptotic cancer therapy under hypoxia.Materials today. Bio · 2026Article
- Perm1 enhances Nrf2-driven antioxidant defense through Keap1 oxidation during myocardial ischemia/reperfusion injury.JCI insight · 2026Article
- TXNIP regulates the proliferation of scar fibroblasts through oxidative stress.European journal of medical research · 2025Article
- p22Nature cardiovascular research · 2025Article
- Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2025Review
- Disulfide stress and its role in cardiovascular diseases.Redox biology · 2024Review
- Thioredoxin1 Binding Metastasis-Associated Lung Adenocarcinoma Transcript 1 Attenuates Inflammation and Apoptosis after Intracerebral Hemorrhage.Aging and disease · 2024Article
- Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases.Redox biology · 2024Review
- N-Acetylcysteine, N-Acetylcysteine Amide, and Thioredoxin Mimetic Peptides Regenerate Mercaptoalbumin and Exhibit Antioxidant Activity.Antioxidants (Basel, Switzerland) · 2024Article
- Insights into the Multifaceted Roles of Thioredoxin-1 System: Exploring Knockout Murine Models.Biology · 2024Review
- Fluorescent Probes for Mammalian Thioredoxin Reductase: Mechanistic Analysis, Construction Strategies, and Future Perspectives.Biosensors · 2023Review
- A Rare Case of Coexisting Mutation in Desmin and Thioredoxin Reductase 2 Genes Causing Dilated Cardiomyopathy.Cureus · 2023Article
- Modulation of Nrf2/HO-1 by Natural Compounds in Lung Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- Thioredoxin 1 promotes autophagy through transnitrosylation of Atg7 during myocardial ischemia.The Journal of clinical investigation · 2023Article
- S-Denitrosylation: A Crosstalk between Glutathione and Redoxin Systems.Antioxidants (Basel, Switzerland) · 2022Review
- Role of Oxidative Stress in Cardiac Dysfunction and Subcellular Defects Due to Ischemia-Reperfusion Injury.Biomedicines · 2022Review
- Article
- Redox signaling, mitochondrial metabolism, epigenetics and redox active phytochemicals.Free radical biology & medicine · 2022Review
- Genome-wide methylation patterns in Marfan syndrome.Clinical epigenetics · 2021Article
- Application of Bulky NHC-Rhodium Complexes in Efficient S-Si and S-S Bond Forming Reactions.Inorganic chemistry · 2021Article
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
Abstract
Myocardial ischemia/reperfusion and heart failure are the major cardiac conditions in which an imbalance between oxidative stress and anti-oxidant mechanisms is observed. The myocardium has endogenous reducing mechanisms, including the thioredoxin (Trx) and glutathione systems, that act to scavenge reactive oxygen species (ROS) and reduce oxidized proteins. The Trx system consists of Trx, Trx reductase (TrxR), and an electron donor, NADPH, where Trx is maintained in a reduced state in the presence of TrxR and NADPH. Trx1, a major isoform of Trx, is abundantly expressed in the heart and exerts its oxidoreductase activity through conserved Cys32 and Cys35, reducing oxidized proteins through thiol disulfide exchange reactions. In this review, we will focus on molecular targets of Trx1 in the heart, including transcription factors, microRNAs, histone deactylases, and protein kinases. We will then discuss how Trx1 regulates the functions of its targets, thereby affecting the extent of myocardial injury caused by myocardial ischemia/reperfusion and the progression of heart 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.