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Ischemia, reactive oxygen species (ROS), and inflammation can trigger pro-apoptotic protein signaling (Bax, Bak) and inhibit anti-apoptotic protein signaling (Bcl-2, Bcl-xL) within cardiomyocytes leading to release of cytochrome c and activation of caspases causing apoptosis. Pro-survival proteins that bind to their respective receptors on the myocyte surface can trigger PI3K/Akt and Ras-Raf-MEK-ERK pathways anti-apoptotic molecular pathways to prevent cell death.
