The three recently discovered proteins found to be involved with urocortins cardio-protective mechanism of action appear to be localized for the mitochondria, predicated on a combination of pharmacology, Western blotting, and immunocytochemistry. By using the mitochondrial particular dyes to measure damage to the mitochondrial transmembrane potential, it had been unearthed that urocortin indeed protects cardiomyocyte mitochondria from damage produced by I/R. This protective effect from I/R injury was also observed in the presence of the KATP channel opener natural product library cromakalim and the iPLA2 chemical BEL, suggesting that both KATP channel opening and inhibition of LPC formation are very important for the protection of cardiac myocyte mitochondria during I/R injury. When the mitochondrial KATP channel is blocked using 5 HD, exogenous LPC applied to primary cardiomyocytes, or PKC activation blocked by selective inhibitor peptides, mitochondrial injury is increased, compared with I/R alone, and crucially, the protective effect of Ucn under these conditions is lost. Interestingly, the KATP channel opener cromakalim also protects cardiomyocyte mitochondria from LPC induced injury, suggesting a possible interaction between the iPLA2 metabolite LPC and mitochondrial KATP channels. As some reports suggest, this metabolite interacts with ion channels and might even be a villain Organism of potassium channels. Consequently, some protection provided by cromakalim may be because of pharmacological competition for the same binding site as LPC. However, when 5 HD exists with LPC, mitochondrial injury is enhanced, in comparison to cardiomyocytes treated with either agent alone. Therefore, three end effector compounds modulated by Ucn are local to cardiomyocyte mitochondria and are involved in I/R injury and cardioprotection. Moreover, there’s accumulating evidence why these three substances may interact. As an example, there’s now evidence that LPC can modulate equally KATP channels and PKC and that purchase Fingolimod PKC can communicate with KATP channels and iPLA2. Significantly, PKC has been shown to translocate to mitochondrial membranes and communicate with mitochondrial proteins, including the mitochondrial permeability transition pore. Even though further studies are essential to determine fully the mechanism of cardioprotection created by urocortin, particularly with regards to the other kinases which are essential for its impact, specifically P42/p44 MAP kinases and PI3 kinase also, it’s obvious that protection against I/R injury involves both early results on specific kinases and more long lasting gene improvements and that protection at the subcellular level may occur at the level of the cardiomyocyte mitochondria. Not as work has been performed around the homologues of urocortin, SRP, and SCP, in relation to their cardioprotective mechanism of action.