Galectin-3 Expression Promotes Pulmonary Hypertension Through Multiple Mechanisms

Abstract

Pulmonary Hypertension is a progressive vascular disease resulting from the tapering of pulmonary arteries causing high pulmonary arterial blood pressure and ultimately right ventricular failure. A defining characteristic of Pulmonary Hypertension is the excessive remodeling of pulmonary arteries that includes increased proliferation, vascular fibrosis and inflammation. There is no outward cure for Pulmonary Hypertension nor are there interventions that effectively impede or reverse pulmonary arterial remodeling, and pulmonary vascular research over the past several decades has sought to identify novel molecular mechanisms to target for therapeutic benefit. Galectin-3 is a carbohydrate binding lectin that is unique for its chimeric structure, comprised of an N-terminal oligomerization domain and a C-terminal carbohydrate-recognition domain. Galectin-3 is a regulator of modifications in cell behavior that contribute to aberrant pulmonary arterial remodeling including cell proliferation, inflammation, and fibrosis, but its role in Pulmonary Hypertension is poorly understood. In this review, we define Galectin-3 and summarize specific topics regarding the role of Galectin-3 expression in the development of Pulmonary Hypertension by providing evidence which supports the ability of Galectin-3 to influence reactive oxygen species production, NADPH enzyme expression, vascular inflammation and vascular fibrosis, all phenomena which contribute to pulmonary arterial remodeling and the development of Pulmonary Hypertension.