ArticleAntioxidants & redox signaling2011
Role of apoptosis signal-regulating kinase-1-c-Jun NH2-terminal kinase-p38 signaling in voltage-gated K+ channel remodeling of the failing heart: regulation by thioredoxin.
Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases.Redox biology · 2024Review
- Cardioprotective Effects of a Selective c-Jun N-terminal Kinase Inhibitor in a Rat Model of Myocardial Infarction.Biomedicines · 2023Article
- TBC1D25 Regulates Cardiac Remodeling Through TAK1 Signaling Pathway.International journal of biological sciences · 2020Article
- Cholecystokinin type B receptor-mediated inhibition of A-type KCell communication and signaling : CCS · 2019Article
- Improvement of vascular dysfunction by argirein through inhibiting endothelial cell apoptosis associated with ET-1/Nox4 signal pathway in diabetic rats.Scientific reports · 2018Article
- p38 MAPK in cardioprotection - are we there yet?British journal of pharmacology · 2015Review
- Hypoxia-dependent reactive oxygen species signaling in the pulmonary circulation: focus on ion channels.Antioxidants & redox signaling · 2015Review
- Redox regulation of ion channels in the pulmonary circulation.Antioxidants & redox signaling · 2015Review
- Coherent functional modules improve transcription factor target identification, cooperativity prediction, and disease association.PLoS genetics · 2014Article
- Thioredoxins, glutaredoxins, and peroxiredoxins--molecular mechanisms and health significance: from cofactors to antioxidants to redox signaling.Antioxidants & redox signaling · 2013Review
- Thioredoxin 1 is essential for sodium sulfide-mediated cardioprotection in the setting of heart failure.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Interacting with thioredoxin-1--disease or no disease?Antioxidants & redox signaling · 2013Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
c-Jun NH(2)-terminal kinase (JNK) and p38 kinase are key regulators of cardiac hypertrophy and apoptosis during pathological stress, but their role in regulating ion channels in the diseased heart is unclear. Thus, we compared the kinase profile and electrophysiological phenotype of the rat ventricle 6-8 weeks after myocardial infarction (MI). Molecular analyses showed that JNK and p38 activities were markedly increased in post-MI hearts, while parallel voltage-clamp studies in ventricular myocytes revealed a characteristic downregulation of transient outward K(+) current (I(to)) density. When post-MI myocytes were treated with JNK or p38 inhibitors, I(to) density increased to control levels. Upregulation of I(to) was also elicited by insulin-like growth factor-1, which decreased JNK/p38 activity in post-MI hearts, and these changes were blocked by the thioredoxin (Trx) reductase inhibitor auranofin. Consistent with activation of JNK-p38 signaling, binding of apoptosis signal-regulating kinase-1 with Trx1 was also markedly decreased post-MI, and was reversed by insulin-like growth factor-1 in an auranofin-sensitive manner. We conclude that expression of ventricular K(+) channels is redox regulated and that chronic impairment of the Trx system in the post-MI heart contributes to I(to) remodeling through sustained activation of apoptosis signal-regulating kinase-1-JNK-p38 signaling. The cardiac Trx system may thus be a novel therapeutic target to reverse or prevent ventricular arrhythmias in the failing heart.
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Registered trials
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