ArticleFree radical biology & medicine2007
Nitrative thioredoxin inactivation as a cause of enhanced myocardial ischemia/reperfusion injury in the aging heart.
Article in Free radical biology & medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 55 citations in OpenAlex.
- Aging might augment reactive oxygen species (ROS) formation and affect reactive nitrogen species (RNS) level after myocardial ischemia/reperfusion in both humans and rats.Age (Dordrecht, Netherlands) · 2013Trial
- Aging might increase myocardial ischemia / reperfusion-induced apoptosis in humans and rats.Age (Dordrecht, Netherlands) · 2012Trial
- Thioredoxin system dysregulation and calpain activation drive myocardial disulfidptosis via pathological disulfide bonds remodeling.Cell death discovery · 2026Article
- Crystallographic mining of ASK1 regulators to unravel the intricate PPI interfaces for the discovery of small molecule.Computational and structural biotechnology journal · 2022Review
- Alda-1 treatment promotes the therapeutic effect of mitochondrial transplantation for myocardial ischemia-reperfusion injury.Bioactive materials · 2021Article
- Intranasal administration of Cytoglobin modifies human umbilical cord‑derived mesenchymal stem cells and improves hypoxic‑ischemia brain damage in neonatal rats by modulating p38 MAPK signaling‑mediated apoptosis.Molecular medicine reports · 2020Article
- Cardiac-specific Mst1 deficiency inhibits ROS-mediated JNK signalling to alleviate Ang II-induced cardiomyocyte apoptosis.Journal of cellular and molecular medicine · 2019Article
- Conditioning-induced cardioprotection: Aging as a confounding factor.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Review
- Interplay between ROS and Antioxidants during Ischemia-Reperfusion Injuries in Cardiac and Skeletal Muscle.International journal of molecular sciences · 2018Review
- Nuclear Factor (Erythroid-Derived 2)-Like 2 and Thioredoxin-1 in Atherosclerosis and Ischemia/Reperfusion Injury in the Heart.Antioxidants & redox signaling · 2017Review
- Myocardial susceptibility to ischaemia/reperfusion in obesity: a re-evaluation of the effects of age.BMC physiology · 2017Article
- Ischemic postconditioning confers cardioprotection and prevents reduction of Trx-1 in young mice, but not in middle-aged and old mice.Molecular and cellular biochemistry · 2016Article
- Loss of myocardial protection against myocardial infarction in middle-aged transgenic mice overexpressing cardiac thioredoxin-1.Oncotarget · 2016Article
- Redox regulation of ion channels in the pulmonary circulation.Antioxidants & redox signaling · 2015Review
- Dickkopf-3 attenuates pressure overload-induced cardiac remodelling.Cardiovascular research · 2014Article
- Thioredoxins, glutaredoxins, and peroxiredoxins--molecular mechanisms and health significance: from cofactors to antioxidants to redox signaling.Antioxidants & redox signaling · 2013Review
- Thioredoxin reductase was nitrated in the aging heart after myocardial ischemia/reperfusion.Rejuvenation research · 2013Article
- Variations in the protein level of Omi/HtrA2 in the heart of aged rats may contribute to the increased susceptibility of cardiomyocytes to ischemia/reperfusion injury and cell death : Omi/HtrA2 and aged heart injury.Age (Dordrecht, Netherlands) · 2013Article
- Interacting with thioredoxin-1--disease or no disease?Antioxidants & redox signaling · 2013Review
- Therapeutic targets in the ASK1-dependent stress signaling pathways.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2012Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Several recent studies have demonstrated that thioredoxin (Trx) is an important antiapoptotic/cytoprotective molecule. The present study was designed to determine whether Trx activity is altered in the aging heart in a way that may contribute to increased susceptibility to myocardial ischemia/reperfusion (MI/R). Compared to young animals, MI/R-induced cardiomyocyte apoptosis and infarct size were increased in aging animals (p<0.01). Trx activity was decreased in the aging heart before MI/R, and this difference was further amplified after MI/R. Trx expression was moderately increased and Trx nitration, a posttranslational modification that inhibits Trx activity, was increased in the aging heart. Moreover, Trx-aptosis-regulating kinase-1 (Trx-ASK1) complex formation was reduced and activity of p38 mitogen-activated protein kinase (MAPK) was increased. Treatment with FP15 (a peroxynitrite decomposition catalyst) reduced Trx nitration, increased Trx activity, restored Trx-ASK1 interaction, reduced P38 MAPK activity, attenuated caspase 3 activation, and reduced infarct size in aging animals (p<0.01). Our results demonstrated that Trx activity is decreased in the aging heart by posttranslational nitrative modification. Interventions that restore Trx activity in the aging heart may be novel therapies to attenuate MI/R injury in aging patients.
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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.