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Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
Published on: September 3, 2020
Salvage of ischemic myocardium: a focus on JNK
1Department of Internal Medicine and Botnar Center for Clinical Research, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. hduplain@hospvd.ch
Insights
Treating myocardial infarction involves restoring blood flow. New strategies aim to prevent heart muscle cell death by targeting the c-Jun N-terminal kinase (JNK) pathway, offering potential cardioprotection.
Area of Science:
- Cardiology
- Molecular Biology
- Cellular Signaling
Background:
- Myocardial infarction (MI) poses significant morbidity and mortality risks.
- Current treatments focus on reperfusion of the occluded coronary artery.
- Preventing ischemic myocardial cell death via intracellular pathways is a crucial complementary approach.
Purpose of the Study:
- To review the role of c-Jun N-terminal kinase (JNK) in cardiac ischemia/reperfusion injury.
- To summarize advances in using JNK inhibitors for myocardial protection.
Main Methods:
- Review of scientific literature on JNK signaling in cardiac ischemia.
- Analysis of studies investigating JNK inhibitors in animal models of myocardial infarction.
Main Results:
- JNK is a key determinant of cardiac cell survival and death during ischemia/reperfusion.
- Several strategies targeting JNK have shown efficacy in reducing infarct size in preclinical models.
Conclusions:
- JNK signaling is a critical target for cardioprotection.
- JNK inhibitors represent a promising therapeutic strategy to limit myocardial damage post-MI.
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.
