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Figure 3. Overview of the JAK/STAT pathway activated after ischemic preconditioning (IP) or ischemia/reperfusion (I/R) injury. Free radical production (reactive oxygen species) is known to mediate the damaging effects of IR. The extent of cardiac myocyte damage after I/R as a result of cell death will depend on the balance and levels of activated STAT1 (pST1) or STAT3 (pST3) modulating pro- and antiapoptotic genes. Agents that act as ROS scavengers such as tempol may also modulate the functional activity of STATs.
