“Junk” inhibition protects the heart from heart attack

Photo by Chelsee Tysoe

Heart attacks are dangerous because of the hypoperfusion, low blood flow, to heart cells and cascaded cell damage caused by reactive oxygen species and cell waste once reperfusion occurs. Researchers of the Scripps Research Institute of Florida found that by inhibiting c-jun-N-terminal Kinase (JNK or “junk”), the ischemic/reperfusion induced cardiomyocyte death could be prevented.

A heart attack causes an occlusion of blood vessels leading to the heart and results in low oxygen delivered to cardiomyocytes. As the cells are delivered less and less oxygen, a switch is made to anaerobic metabolism. Following, the cell membranes are broken down by lipases and calcium is allowed to freely rush into the cell. This causes the generation of free radicals (FR), reactive oxygen species (ROS), and the release of toxins/apoptotic factors into the cell (not to mention mitochondrial dysfunction). This dangerous process is exacerbated by the treatment of ischemia by restoring blood flow. This is because the toxins, FRs, and ROSs are rapidly shuttled to the cells and nearby tissues causing cell death.

Previous studies have shown that JNK plays a major role in the (dysfunctional) mitochondrial signaling to release FRs and ROSs; therefore, this group tested the effect of blocking that signaling or inhibiting JNK all together in vivo using rats.

Inducing heart attack in the rats and introducing 5 mg/kg of SR-3306 (JNK inhibitor) reduced ischemic/reperfusion injury by 34%. Cardiomyocyte apoptosis was also seen as reduced 4-fold by SR-3306.

Blocking JNK signaling via mitochondria effectively reduced heart attack damage to heart cells and the surrounding tissue. It seems blocking this junk induced pathway will prove useful in protecting hearts and saving lives.

Reference:
Jeremy W. Chambers, Alok Pachori, Shannon Howard, Sarah Iqbal, Philip V. LoGrasso. Inhibition of JNK Mitochondrial Localization and Signaling is Protective Against Ischemia-
Reperfusion Injury in Rats. The Journal of Biological Chemistry, 2012.
http://dx.doi.org/10.1074/jbc.M112.406777

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