Free leptin, carotid plaque phenotype and relevance to related symptomatology: Insights from the OPAL-Lille carotid endarterectomy study

摘要

Stroke, a major public health issue, occurs, in 50% of cases, subsequently to the rupture of an unstable atherosclerotic carotid artery plaque [1]. Plaque mechanical stability is related to its histological features: matrix (collagen, lipid...) and cellular components (macro-phages, vascular smooth muscle cells, VSMC) [2J. VSMC, the major cell type in atherosclerotic plaques responsible for plaque progression, are more recently seen to promote plaque stability thus preventing stroke [3]. Serum leptin, an adipose tissue-derived cytokine, circulates as a free biologically active form and as a bound form to its soluble ObR receptor. Initially described as a central satiety signal, leptin is assumed to modify vessel wall homeostasis via multiple effects exerted through an interaction with its ObR receptors expressed on vascular cell surface [4]. In patients with overt atherosclerotic cardiovascular diseases, the association between total leptin concentrations and various cardiovascular risks has yielded conflicting results.