Cardioprotection includes all mechanisms and means that contribute to the preservation of theheart by reducing or even preventing myocardial damage.^[1]

Cardioprotection encompasses several regimens that have shown to preserve function and viability ofcardiac muscle cell tissue subjected toischemic insult orreoxygenation.

Cardioprotection includes strategies that are implemented:

• before anischemic event (preconditioning, PC),
• during an ischemic event (perconditioning, PerC),
• after the event and during reperfusion (postconditioning, PostC).^[2]

These strategies can be further stratified by performing the intervention locally or remotely, creating classes of conditioning known as remoteischemic PC (RIPC), remote ischemic PostC and remote ischemic PerC.^[2] Classical (local)preconditioning has an early phase with an immediate onset lasting 2–3 hours that protects againstmyocardial infarction.^[3] The early phase involvespost-translational modification of preexisting proteins, brought about by the activation ofG protein-coupled receptors as well as downstreamMAPK's andPI3/Akt. These signaling events act on theROS-generatingmitochondria, activatePKCε and the Reperfusion Injury Salvage Kinase (RISK) pathway, preventingmitochondrial permeability transition pore (MTP) opening.^[4] The late phase with an onset of 12–24 hours that lasts 3–4 days and protects against bothinfarction and reversible postischemiccontractile dysfunction, termedmyocardial stunning.^[5][6][7] This phase involves the synthesis of new cardioprotectiveproteins stimulated bynitric oxide (NO),Reactive oxygen species (ROS) andadenosine acting on kinases such asPKCε andSrc, which in turn activategene transcription and upregulation of late PC molecular players (e.g.,antioxidant enzymes,iNOS).^[8]

A role for PKCε in more contemporary cardioprotection strategies including RIPC,^[9] local PostC,^[10] and remote PostC^[11] have been either demonstrated or suggested. It was shown that PKCε translocates from thecytosolic to the particulate fraction upon RIPC induction and that the protection conferred by RIPC can be inhibited with the PKC inhibitorchelerythrine^[12][13] Similarly, in models of local PostC,phosphorylation and activation of PKCε has been shown to be induced and PKCε inhibition attenuated the beneficial effects of these regimens.^[14][15] A recent study showed that blockingHsp90 function withgeldanamycin inhibits PostC protection and PKCε translocation.^[16] Additional studies are required to investigate a role for PKCε in remote PostC and PerC, as this has not been conclusively demonstrated.

Cardioprotective strategies are studied for their potential to reduce heart damage in conditions like heart attack or surgery involving reperfusion.

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