Mitochondria as a target of cardioprotection in models of preconditioning.

Over the recent years the view on mitochondria in the heart as a cellular powerhouse providing ATP supply needed to sustain contractile function, basal metabolic processes, and ionic homeostasis has changed radically. At present it is known that dysfunctions of these organelles are essential in the development of a large number of diseases, including cardiovascular diseases. Moreover, mitochondria are considered to be a very promising target of endogenous strategies that are essential in the protection of the myocardium from acute ischemia/reperfusion injury. These strategies including ischemic preconditioning, remote ischemic preconditioning as well as the acute phase of streptozotocin-induced diabetes mellitus, provide a similar effect of protection. Alterations observed in the functional and structural properties of heart mitochondria caused by short-term pathological impulses are associated with endogenous cardioprotective processes. It seems that the extent of mitochondrial membrane fluidization could be an active response mechanism to injury with a subtle effect on membrane-associated processes which further affect the environment of the whole organelle, thus inducing metabolic changes in the heart. In this review article, we provide an overview of endogenous protective mechanisms induced by hypoxic, pseudohypoxic and ischemic conditions with special consideration of the role of heart mitochondria in these processes.