Ischemia and Reperfusion Protection
Heart failure (HF) is the final stage of pre-existing cardiovascular diseases. In an aging population, as in the EU community, HF is a serious problem for the society, greatly detrimental for the quality of life. Despite technological and pharmacological advances fostering early diagnosis and therapeutic interventions, HF is the only major cardiovascular disease whose prevalence and incidence are increasing. The ischemic heart disease is the leading cause of HF. After an acute myocardial infarction, reperfusion injury occurs with a central role for mitochondrial dysfunction.
Both ischemic pre- and post-conditioning trigger the activation of intracellular signaling pathways, which converge on mitochondria and limit cell death. These pathways include the survival kinases of RISK (Reperfusion Injury Salvage kinases) and the elements of SAFE (Survival Activating Factor Enhancement). To fully understand the molecular mechanisms of cardioprotection is essential to design future clinical trials.
In the attempt to define the signaling mechanisms that address myocardial tissue towards a cardioprotective phenotype and to validate the efficacy of new molecular targets, we are studying the vasodilating and cardioprotective effects of peptide hormones derived from Chromogranin A (Vasostatin and Catestatin), or belonging to the GHRH family, with particular attention to the intracellular pathways involved.