The cellular mechanisms involved in Ischemic Preconditioning. IPC, IPost, or pharmacological agents initiates the release of G-protein-coupled receptor (GPCR) agonists which bind to the receptor and activate numerous signaling pathways. Phosphatidylinositol-3-kinase (PI3K) and Ras activation can lead to activation of a number of downstream molecules such as Akt, protein kinase C (PKC), extracellular regulated kinase (ERK), nitric oxide synthase (NOS), and inactivation of glycogen synthase kinase-3β (GSK-3β). These converge to activate the mitochondrial ATP-dependent potassium channel (KATP), closing the mitochondrial permeable transition pore (mPTP) resulting in protection from IRI [67].
