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Cardioprotection refers broadly to all mechanisms—physiological adaptations, pharmacologic treatments, device-based interventions—that help preserve heart function by reducing or preventing damage from events such as ischemia-reperfusion. This includes preconditioning before an ischemic event, interventions during ischemia/reperfusion (like postconditioning), and various drug therapies targeting cellular survival pathways. While many molecules play roles in these processes—such as kinases in the RISK pathway or inhibitors like cyclosporin A—the term “cardioprotection” does *not* denote any one molecular entity but instead describes the overall goal/outcome achieved through diverse means[1][2][4].
Mechanisms involved in cardioprotective strategies include: - Inhibition of mitochondrial permeability transition pore opening (e.g., cyclosporine A)[9] - Activation of G protein-coupled receptors leading to pro-survival kinase signaling pathways such as RISK and SAFE pathways[1][2] - Modulation of nitric oxide signaling and reactive oxygen species production[1]
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