ArticleMedical science monitor : international medical journal of experimental and clinical research2020
Peroxiredoxin2 (Prdx2) Reduces Oxidative Stress and Apoptosis of Myocardial Cells Induced by Acute Myocardial Infarction by Inhibiting the TLR4/Nuclear Factor kappa B (NF-κB) Signaling Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 36 citations in OpenAlex.
- Peroxiredoxins in the kidney: a Jekyll and Hyde existence in disease pathogenesis.Renal failure · 2026Review
- Salidroside attenuates myocardial ischemia‑reperfusion‑induced oxidative stress and ferroptosis by promoting USP11‑mediated deubiquitination of PRDX2.International journal of molecular medicine · 2026Article
- Ubiquitination-mediated PRDX2 alleviates intervertebral disc degeneration via restraining TBHP-induced nucleus pulposus cell apoptosis, ferroptosis and ECM degradation.Journal of inflammation (London, England) · 2026Article
- Molecular characterization of bovine viral diarrhea virus and host genetic immune and biochemical responses in diarrheic buffalo calves.Scientific reports · 2026Article
- Spatiotemporal dynamics of reactive oxygen species: implications for cellular homeostasis and redox therapies.Cellular & molecular biology letters · 2026Review
- Plasma-Derived Extracellular Vesicles Inhibit Lipopolysaccharide-Induced Apoptosis and Oxidative Stress in Human AC16 Cardiomyocytes.Current issues in molecular biology · 2026Article
- NF-Frontiers in cardiovascular medicine · 2026Review
- Overexpression of PRDX2 alleviates chronic thromboembolic pulmonary hypertension by modulating inflammation and mitophagy.Scientific reports · 2025Article
- Harpagide Confers Protection Against Acute Lung Injury Through Multi-Omics Dissection of Immune-Microenvironmental Crosstalk and Convergent Therapeutic Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Amitriptyline increases food intake via prdx-2 without altering other physiological parameters in C. elegans under a modified bacterial diet.Scientific reports · 2025Article
- Toxicity Responses from Tributyltin Chloride on Haarder (Current issues in molecular biology · 2025Article
- Uncovering key biomarkers, potential therapeutic targets and development of deep learning model in heart failure.PloS one · 2025Article
- Correlation analysis between the expression of serum microRNA-665 and the degree of coronary artery stenosis and major adverse cardiovascular events in patients with acute myocardial infarction.Journal of cardiothoracic surgery · 2024Article
- Secretome profiling reveals acute changes in oxidative stress, brain homeostasis, and coagulation following short-duration spaceflight.Nature communications · 2024Article
- Article
- Cardiovascular Toxicity of Antineoplastic Treatments in Hematological Diseases: Focus on Molecular Mechanisms to Improve Therapeutic Management.Journal of clinical medicine · 2024Review
- Integrated analysis and validation of ferroptosis-related genes and immune infiltration in acute myocardial infarction.BMC cardiovascular disorders · 2024Article
- Data independent acquisition reveals in-depth serum proteome changes in uremic pruritus.Frontiers in physiology · 2024Article
- Modified Si Miao Powder granules alleviates osteoarthritis progression by regulating M1/M2 polarization of macrophage through NF-κB signaling pathway.Frontiers in pharmacology · 2024Article
- A review on regulation of DNA methylation during post-myocardial infarction.Frontiers in pharmacology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Peroxiredoxin2 (Prdx2) is an endogenous peroxidase and has been found to reduce the oxidative burden in cells and thereby reduce cell damage and apoptosis. Therefore, the purpose of this study was to investigate the effect of Prdx2 on the oxidative level and apoptosis of myocardial cells after acute myocardial infarction (AMI). MATERIAL AND METHODS We constructed an AMI model for Sprague-Dawley rats by ligating the left anterior descending coronary artery. We determined the effect of Prdx2 on AMI by detecting changes in Prdx2 in myocardial tissue via western blot and qRT-PCR. In addition, we used recombinant Prdx2 protein to treat rats and detect changes in oxidative stress and apoptosis in rat myocardial tissue to verify the protective effect of Prdx2 on the rat heart. RESULTS The protein and mRNA expression of Prdx2 in myocardial tissue of rats in the AMI group was significantly lower than that in the control group. The oxidative and apoptotic levels of myocardial tissue in Prdx2-administered rats were significantly improved compared to the non-administered group, which was manifested by a decrease in reactive oxygen species (ROS) levels and a decrease in the expression of the caspase family. In addition, Prdx2 also inhibited p65 phosphorylation in myocardial tissues and inhibited TLR4/NF-kappaB signaling pathway activity. CONCLUSIONS The expression of Prdx2 was decreased in myocardial tissue after AMI. Prdx2 can reduce apoptosis and ROS caused by AMI by inhibiting the TLR4/NF-kB signaling pathway, thereby reducing myocardial injury caused by AMI.
Indexed as
Identifiers
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.