Role of temperature in myocardial ischemic injury and protection by conditioning

Organ temperature and ischemia/reperfusion injury (IRI) are strictly linked. It is well known that deep/profound hypothermia can improve cardioplegia induced cardiac preservation. Also mild/moderate hypothermia induces myocardial protection against IRI in beating hearts. Here we will focus on some mechanisms of cardioprotection induced by hypothermia. In particular, we will analyze the effects of hypothermia on heart metabolism, cytosolic calcium, and oxidation/nitrosation processes. The role of inflammation, extracellular matrix processing, genetic, and epigenetic effects in mild hypothermia will be also analyzed. Recent advances on miRNA, exosomes, and extracellular vesicles controlled by temperature variation will be discussed. Particular emphasis will be given to the procedures of conditioning (pre, per and postconditioning and remote conditioning) obtained with thermic and/or ischemic stimuli. In this context hyperthermic processes also play an important protective role. From the analyzed studies, it emerges that temperature is an important variable affecting IRI that deserves to be strictly controlled and eventually modified to amplify the efficacy of cardioprotective strategies. Nevertheless, more in depth studies are necessary to understand the mechanisms of protection induced by thermic therapy alone and in association with other cardioprotective interventions. More in depth investigation into the mechanistic signaling that lead to temperature triggered protection could individuate crucial targeting molecules, representing strategic knowledge to promote a better therapeutic efficacy and a lower cardiovascular risk in the setting of myocardial ischemia/reperfusion.