Date du seminaire
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Arterial calcification has long been thought to be a passive, degenerative process. In contrast, severalworks over the last two decades have established that AC results from a highly-regulated process sharing many similarities with bone tissue formation. The incidence of AC in atherosclerotic lesions is extremely high and AC has been shown to increase the cardiovascular morbidity and mortality independently of other cardiovascular risk factors.

AC is particularly associated with diabetes and chronic kidney disease. Its presence is systemic and affects various vascular beds. The mechanisms underlying its formation involve a wide and complex interplay of inflammatory, metabolic and genetic dysregulations leading to hydroxyapatite cristal deposit and cellular reprogramming. The clinical impact of AC is massive and currently there is no treatment that halts or reverse AC. The proposed presentation will discuss the mechanisms of AC, its clinical consequences and potential therapeutic targets. Setting up a tranlationnal project dedicated to AC treatment, as the one that is currently underway in the ENSAM, is warranted.


Illustration of calcification of lower limb arteries (left) and stent fracture placed on a calcified lesion (right)


Dr. Jean-Michel DAVAINE

Chirurgien vasculaire à l'Hôpital Pitié-Salpêtrière