Author(s)

Ivica Bošnjak^1*, Dražen Bedeković², Kristina Selthofer-Relatić^1,3, Ines Bilić-Ćurčić^1,4

¹Clinic of Internal Medicine, Department of Cardiovascular Disease and Intensive Care, University Hospital Centre Osijek, Osijek, Croatia.
²Department of Internal Medicine, General Hospital Nasice, Nasice, Croatia.
³Department of Internal Medicine and Medical Ethics, School of Medicine, University Josip Juraj Strossmayer, Osijek, Croatia.
⁴Department of Pathophysiology, School of Medicine, University Josip Juraj Strossmayer, Osijek, Croatia.

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.

Galectin-3, Atherosclerosis, Coronary Artery Disease, Coronary Heart Disease, Macrophages, Heart Failure

Bošnjak, I. , Bedeković, D. , Selthofer-Relatić, K. and Bilić-Ćurčić, I. (2017) Galectin-3: A Heart Failure Biomarker as Sign of Active Coronary Heart Disease. World Journal of Cardiovascular Diseases, 7, 373-379. doi: 10.4236/wjcd.2017.711035.