Molecular background and practical therapeutic implications of postconditioning myocardial tissue in a mice model of diabetes and the metabolic syndrome.

As the prevalence of the MS rises rapidly and the components of the MS increase the overall cardiovascular risk synergistically, interest for this syndrome is growing rapidly. The MS leads to very specific cardiomyocyte changes, and as the natural course of the MS is detrimental, it necessitates a tailored approach with correction of the individual risk factors and prevention of the hypertrophic and inflammatory stimuli.

 Although IPreC fails to protect the diabetic heart against ischemic events, we have shown that IPostC is still beneficial at short and long term, both improving functional outcome and infarct size.  New pharmacological insights should enable us to reactivate endogenous cardioprotective pathways in this high risk population and to apply it in cardiovascular interventions.