Abstract
Atherosclerosis is characterized by the accumulation of cholesterol esters, macrophages and fibrous elements on the inner artery wall. This process begins with accumulation of plasma lipoproteins on the inner wall of the artery, which leads to changes in the passage and elasticity of the blood vessels. Monocytes penetrating the arterial wall transforms into macrophages which digest cholesterol and form foam cells which is one of the first steps in atherosclerotic process. Activation of macrophages is affected by galectin-3, a β-galactoside-binding lectin which is also involved in cardiac remodeling. Cardiac matrix remodeling is the ultimate result of macrophages proliferation and chemotaxis, neutrophil extravasation, oxidative stress, apoptosis, angiogenesis, fibroblast proliferation and deposition of collagen. Studies show that elevated levels of galectin 3 within atherosclerotic lesions in humans are closely related to the development of a disease itself. With this review, we want to demonstrate the correlation between galectin-3 which is precipitated in atherosclerotic plaque and has an influence on the development of cardiovascular diseases and its role in the prognosis of recovery in cardiac patients.
Highlights
Atherosclerosis is systematic inflammatory disease which affects major arteries including coronary arteries
It is only a matter of time before galectin-3 becomes a reality in everyday clinical practice
As one of the new markers for heart failure, galectin-3 is mentioned in the new ESC guidelines for the heart failure treatment
Summary
Rupture of such lesion results in thrombus formation and vessel lumen obstruction causing myocardial infarction, cerebral insult or peripheral artery disease. Galectin-3 (Gal-3) is a member of a galectin family involved in numerous physiological and pathological processes such as inflammation and formation of fibrous tissue [2]. It is found in a wide range of tissues and is essential for normal macrophage functioning [3] [4]. Gal-3 level is much higher in patients with unstable coronary disease, which leads to conclusion that Gal-3 can be involved in atherosclerotic plaque destabilization [7]
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