Literature DB >> 17089887

Salvage of ischemic myocardium: a focus on JNK.

Hervé Duplain1.   

Abstract

Myocardial infarction is a problem of utmost clinical significance, associated with an important morbidity and mortality. Actual treatment of this affection is focusing on the reperfusion of the occluded coronary-artery. A complementary approach would be to prevent the death of the ischemic myocardium by interacting with detrimental intracellular pathways. Several strategies have been successfully used to reduce the size of myocardial infarction in animal models. In this article, we will focus on the c-Jun N-terminal kinase (JNK), a member of the mitogen-activated (MAPK) protein kinase family and an important determinant of cell survival/death. We will review the role of JNK in cardiac ischemia/reperfusion and summarize recent advances in the use of JNK inhibitors to protect the myocardium.

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Year:  2006        PMID: 17089887     DOI: 10.1007/978-0-387-34817-9_14

Source DB:  PubMed          Journal:  Adv Exp Med Biol        ISSN: 0065-2598            Impact factor:   2.622


  6 in total

1.  p21-activated kinase improves cardiac contractility during ischemia-reperfusion concomitant with changes in troponin-T and myosin light chain 2 phosphorylation.

Authors:  Michelle M Monasky; Domenico M Taglieri; Bindiya G Patel; Jonathan Chernoff; Beata M Wolska; Yunbo Ke; R John Solaro
Journal:  Am J Physiol Heart Circ Physiol       Date:  2011-10-28       Impact factor: 4.733

2.  c-Jun N-terminal kinase (JNK-1) confers protection against brief but not extended ischemia during acute myocardial infarction.

Authors:  Jianqin Wei; Weiwen Wang; Ines Chopra; Hui Fang Li; Christopher J Dougherty; Jennipher Adi; Nikhil Adi; Huilan Wang; Keith A Webster
Journal:  J Biol Chem       Date:  2011-02-15       Impact factor: 5.157

3.  BGP-15, a PARP-inhibitor, prevents imatinib-induced cardiotoxicity by activating Akt and suppressing JNK and p38 MAP kinases.

Authors:  Zsolt Sarszegi; Eszter Bognar; Balazs Gaszner; Attila Kónyi; Ferenc Gallyas; Balazs Sumegi; Zoltan Berente
Journal:  Mol Cell Biochem       Date:  2012-02-14       Impact factor: 3.396

4.  Synthesis, biological evaluation, and molecular modeling of 11H-indeno[1,2-b]quinoxalin-11-one derivatives and tryptanthrin-6-oxime as c-Jun N-terminal kinase inhibitors.

Authors:  Igor A Schepetkin; Andrei I Khlebnikov; Andrei S Potapov; Anastasia R Kovrizhina; Vladislava V Matveevskaya; Maxim L Belyanin; Dmitriy N Atochin; Svitlana O Zanoza; Nadiya M Gaidarzhy; Sergiy A Lyakhov; Liliya N Kirpotina; Mark T Quinn
Journal:  Eur J Med Chem       Date:  2018-10-12       Impact factor: 6.514

Review 5.  c-Jun N-Terminal Kinases (JNKs) in Myocardial and Cerebral Ischemia/Reperfusion Injury.

Authors:  Maria Shvedova; Yana Anfinogenova; Elena N Atochina-Vasserman; Igor A Schepetkin; Dmitriy N Atochin
Journal:  Front Pharmacol       Date:  2018-07-05       Impact factor: 5.810

Review 6.  Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation.

Authors:  Nina D Anfinogenova; Mark T Quinn; Igor A Schepetkin; Dmitriy N Atochin
Journal:  Cells       Date:  2020-10-24       Impact factor: 6.600

  6 in total

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