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Quit smoking to outsmart atherogenesis: Molecular mechanisms underlying clinical evidence

      Atherosclerosis is a multifactorial pathological process, during which the physiological composition of arterial walls is structurally and functionally altered. The atheroma growth - accumulation of fibro-adipose and degenerative material in the artery walls – leads to the stiffening of vessels and the narrowing of the lumen, limiting the blood flow. Such reduction of blood flow represents only the initial complication of the formation of the atherosclerotic plaque whereas the persistence of the insult, with the hemodynamic instability that characterizes the atherosclerotic artery, can induce evolution of the plaque versus an instable phenotype with major vulnerability and probability of rupture [
      • Novak J.
      • Olejnickova V.
      • Tkacova N.
      • et al.
      Mechanistic role of MicroRNAs in coupling lipid metabolism and atherosclerosis.
      ]. The atherosclerotic plaque rupture leads to the exposure of the highly thrombogenic necrotic core material, with subsequent platelet activation and formation of thrombi that can block blood flow in loco, or break away and enter in the bloodstream, obstructing other vessels with smaller diameter. Therefore, the atherosclerotic process can cause coronary artery disease (CAD), ischemic stroke, and peripheral artery disease, representing a major life-threatening disorder.

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