@article{ATM4771,
author = {Gabriela Suarez and Gary Meyerrose},
title = {Heart failure and galectin 3},
journal = {Annals of Translational Medicine},
volume = {2},
number = {9},
year = {2014},
keywords = {},
abstract = {Innovations in medical diagnosis and treatment have led to prolongation of life of patients. Increasing the life expectancy of cardiac patients and thereby increasing the prevalence of heart failure (HF). Currently more than one million hospital admissions per year are due to HF and it has been estimated that the cost is approximately \$39 billion annually in the U.S. There are two pathophysiologic myocardial mechanisms that cause HF: systolic dysfunction and diastolic dysfunction. Normal cardiac aging is characterized by morphological and structural changes that increase cardiomyocyte size, increased number of apoptosis with decreased number in myocytes, increased collagen deposition, and functional changes at cellular level. All these factors contribute to fibrotic remodeling that leads to LV diastolic stiffness, which ultimately leads to impaired diastolic function. At the same time it has been shown that galectin-3, a soluble β-galactoside-binding protein secreted by activated macrophages, promotes cardiac fibroblast proliferation, collagen deposition, and ventricular dysfunction. In this paper we review the prognostic value of galectin-3 as an independent predictor of mortality in patients with moderate to advanced chronic HF (CHF).},
issn = {2305-5847}, url = {https://atm.amegroups.org/article/view/4771}
}