A peptide inhibitor of c-Jun NH2-terminal kinase reduces myocardial ischemia-reperfusion injury and infarct size in vivo.

@article{Milano2007API,
  title={A peptide inhibitor of c-Jun NH2-terminal kinase reduces myocardial ischemia-reperfusion injury and infarct size in vivo.},
  author={Giuseppina Milano and Sandrine Morel and Christophe Bonny and Michele Samaja and Ludwig Karl von Segesser and Pascal Nicod and Giuseppe Vassalli},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2007},
  volume={292 4},
  pages={
          H1828-35
        }
}
The c-Jun NH(2)-terminal kinase (JNK) pathway of the mitogen-activated protein kinase (MAPK) signaling cascade regulates cell function and survival after stress stimulation. Equally robust studies reported dichotomous results suggesting both protective and detrimental effects of JNK during myocardial ischemia-reperfusion (I/R). The lack of a highly specific JNK inhibitor contributed to this controversy. We recently developed a cell-penetrating, protease-resistant peptide inhibitor of JNK, d… 
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c-Jun N-Terminal Kinases (JNKs) in Myocardial and Cerebral Ischemia/Reperfusion Injury
TLDR
According to reviewed literature, JNKs represent promising therapeutic targets for protection of the brain and the heart against ischemic stroke and myocardial infarction, respectively, but different members of the JNK family exert diverse physiological properties which may not allow for systemic administration of non-specific JNK inhibitors for therapeutic purposes.
Inhibition of JNK Aggravates the Recovery of Rat Hearts after Global Ischemia: The Role of Mitochondrial JNK
TLDR
In the present study, it is sought to examine whether inhibition of JNK by SU3327, a specific JNK inhibitor that inhibits upstream JNK signaling rather than the kinase activity of J NK, improves cardiac function and reduces heart damage during IR.
c-Jun N-terminal Kinase (JNK-1) Confers Protection against Brief but Not Extended Ischemia during Acute Myocardial Infarction*
TLDR
A novel role is defined for JNK-1 as a conditional survival kinase that protects the heart against brief but not protracted ischemia.
PKCbeta modulates ischemia-reperfusion injury in the heart.
TLDR
The data implicate PKCbeta in I/R-mediated myocardial injury, at least in part via phosphorylation of JNK, and suggest that blockade of PKC beta may represent a potent strategy to protect the vulnerable myocardium.
Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation
TLDR
The role of MAPK activation during myocardial IR injury as it occurs during heart transplantation is reviewed and p38 MAPK inhibition improves cardiac function after cold storage, rewarming and reperfusion.
Role of c-Jun N-terminal Kinase in the Regulation of Vascular Tone
TLDR
The results suggest that JNK signaling plays a role in the regulation of vascular tone.
Activation of p38 mitogen-activated protein kinase abolishes insulin-mediated myocardial protection against ischemia-reperfusion injury.
TLDR
It is concluded that insulin protects myocardium against ischemia-reperfusion injury when given prior to ischemIA or reperfusion, and activation of p38 MAPK abolishes insulin's cardioprotective effect.
Effect of cell permeable peptide of c-Jun NH2-terminal kinase inhibitor on the attenuation of renal ischemia-reperfusion injury in pigs.
Activation of p 38 mitogen-activated protein kinase abolishes insulin-mediated myocardial protection against ischemia-reperfusion injury
TLDR
It is concluded that insulin protects myocardium against ischemiareperfusion injury when given prior to ischemia or reperfusion, and activation of p38 MAPK abolishes insulin’s cardioprotective effect.
The ubiquitin ligase MuRF1 protects against cardiac ischemia/reperfusion injury by its proteasome-dependent degradation of phospho-c-Jun.
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