ReviewJournal of cardiovascular pharmacology and therapeutics2017
The Emerging Role of Thioredoxin-Interacting Protein in Myocardial Ischemia/Reperfusion Injury.
Review in Journal of cardiovascular pharmacology and therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 50 citations in OpenAlex.
- Mutations in the Txnip PPXY motifs protect against myocardial infarction despite enhanced protein stability.American journal of physiology. Heart and circulatory physiology · 2026Article
- A new chromosome-level genome assembly for western painted turtle Chrysemys picta bellii, a model for extreme physiological adaptations.BMC genomics · 2026Article
- NLRP3 inflammasome pathway activation is associated with cardiac remodeling, gut microbiota dysbiosis, and dietary protein restriction in a rat heart failure model: an integrative exploratory analysis.Frontiers in genetics · 2026Article
- Review
- Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2025Review
- N-Terminomic Identification of Intracellular MMP-2 Substrates in Cardiac Tissue.Journal of proteome research · 2024Article
- METTL3 Modulates TXNIP Expression to Affect the Activation of NLRP3 Inflammasome in Hepatic Cells Under Oxygen-Glucose Deprivation/Reperfusion Injury.Inflammation · 2024Article
- Rutin attenuates ensartinib-induced hepatotoxicity by non-transcriptional regulation of TXNIP.Cell biology and toxicology · 2024Article
- Geniposide alleviates post-myocardial infarction-induced pyroptosis by modulating the thioredoxin-interacting protein/NLRP3 signaling pathway.CytoJournal · 2024Article
- TXNIP aggravates cardiac fibrosis and dysfunction after myocardial infarction in mice by enhancing the TGFB1/Smad3 pathway and promoting NLRP3 inflammasome activation.Acta biochimica et biophysica Sinica · 2023Article
- Myocardial Glutathione Synthase and TRXIP Expression Are Significantly Elevated in Hypertension and Diabetes: Influence of Stress on Antioxidant Pathways.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Article
- Various Expressions ofBiomolecules · 2023Article
- Chronic cold stress-induced myocardial injury: effects on oxidative stress, inflammation and pyroptosis.Journal of veterinary science · 2023Article
- Pharmacological Basis for Abrogating Myocardial Reperfusion Injury Through a Multi-Target Combined Antioxidant Therapy.Clinical pharmacokinetics · 2022Review
- Role of Oxidative Stress in Cardiac Dysfunction and Subcellular Defects Due to Ischemia-Reperfusion Injury.Biomedicines · 2022Review
- Cytotoxic and Radiosensitising Effects of a Novel Thioredoxin Reductase Inhibitor in Brain Cancers.Molecular neurobiology · 2022Article
- Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review).International journal of molecular medicine · 2022Review
- Thioredoxin-Interacting Protein in Cancer and Diabetes.Antioxidants & redox signaling · 2022Review
- The NLRP3 Inflammasome as a Novel Therapeutic Target for Cardiac Fibrosis.Journal of inflammation research · 2022Review
- ROS: Basic Concepts, Sources, Cellular Signaling, and its Implications in Aging Pathways.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Myocardial ischemia/reperfusion injury represents a major threat to human health and contributes to adverse cardiovascular outcomes worldwide. Despite the identification of numerous molecular mechanisms, understanding of the complex pathophysiology of this clinical syndrome remains incomplete. Thioredoxin-interacting protein (Txnip) has been of great interest in the past decade since it has been reported to be a critical regulator in human diseases with several important cellular functions. Thioredoxin-interacting protein binds to and inhibits thioredoxin, a redox protein that neutralizes reactive oxygen species (ROS), and through its interaction with thioredoxin, Txnip sensitizes cardiomyocytes to ROS-induced apoptosis. Interestingly, evidence from recent studies also suggests that some of the effects of Txnip may be unrelated to changes in thioredoxin activity. These pleiotropic effects of Txnip are mediated by interactions with other signaling molecules, such as nod-like receptor pyrin domain-containing 3 inflammasome and glucose transporter 1. Indeed, Txnip has been implicated in the regulation of inflammatory response and glucose homeostasis during myocardial ischemia/reperfusion injury. This review attempts to make the case that in addition to interacting with thioredoxin, Txnip contributes to some of the pathological consequences of myocardial ischemia and infarction through endogenous signals in multiple molecular mechanisms.
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What Socratic 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 Socratic graph.