Élastokines : facteurs de survie cardiaque

Neoangiogenesis, the formation of new blood capillaries from pre-existing vessels, plays a central role in a number of physiological and pathological processes. Neoangiogenesis is tightly regulated by a myriad of components exhibiting pro-angiogenic or antiangiogenic properties. Nitric oxide is one of the major molecules initiating this process and its production is under the control of intracellular enzymes, the nitric oxide synthases, which are themselves regulated by a protein kinase B, for example, AKT. With ageing, neoangiogenesis is impaired, a condition that contributes to delayed wound repair, neurodegeneration and renal diseases and is particularly detrimental during the revascularization of the ischemic heart or collateral vessels development in cardiovascular diseases. The cardiovascular system, notably the heart, is affected by structural, molecular, cellular and functional changes with age. These modifications diminish the ability of the aged heart to adapt to a number of stress and reinforce not only the sensitivity of aged subjects to myocardial ischemia but also its frequency with ageing. With ageing the elastin content of heart decreases to the detriment of collagen fibres and microfibrils, which are principally composed of fibrillin-1, a constituent that increases in cardiac fibrosis following myocardial ischemia. Elastin and elastokines through their pro-angiogenic, cardioprotective and regenerative properties may contibute to the revascularization and remodeling processes of ischemic tissue after a myocardial infarction. They may also constitute an alternative way to the conventional angiogenic and cellular therapeutic strategies for myocardial repair.