Abstract
Pulmonary arterial hypertension (PAH) is multifactorial disadptive disease with poor clinical outcomes associated with increased pulmonary artery pressure resulting in primary small-to-moderate pulmonary artery remodeling. Numerous factors, including smooth muscle cell proliferation, vasospasm, vascular fibrosis and occlusion, direct vascular injury and inflammation, impaired repair of vasculature, are involved in the pathogenesis of PAH. It has been suggested that galectin-3 as a biomarker of excessive fibrosis and inflammation can be useful predictor of both severity and prognosis in patient with PAH. The short communication is reported that elevated Gal-3 levels were found in majority patients with PAH depending on clinical status and of the disease. Although elevated Gal-3 levels were associated with a higher risk of all-cause mortality, cardiovascular mortality, and right ventricle heart failure, the value of this biomarker in PAH patients at high risk stratification is uncertain and requires to be investigated in large clinical trials.
Highlights
Pulmonary arterial hypertension (PAH) is a steadily progressive maladaptive disease with potentially fatal consequences that has been demonstrated increasing prevalence worldwide (Lai, Y.C. et al, 2014)
Nature evolution of PAH closely related to vascular remodeling and endothelial dysfunction that lead to obstruction of small-to-moderate pulmonary arteries, resulting in increased pulmonary artery pressures and pulmonary vascular resistance associated with uncoupling oxygen supply and blood saturation, hypoxia, right ventricle heart failure and multi organ insufficiency
There were found numerous factors, which contributed to several faces of the PAH including smooth muscle cell proliferation, vasospasm, vascular fibrosis and occlusion, direct vascular injury and inflammation, impaired repair of vasculature (Yu, J. et al, 2013)
Summary
Pulmonary arterial hypertension (PAH) is a steadily progressive maladaptive disease with potentially fatal consequences that has been demonstrated increasing prevalence worldwide (Lai, Y.C. et al, 2014). All these factors corresponding to imbalance of vasodilators (nitric oxide - NO, and prostacyclin) and vasoconstrictors (endothelin-1 - ET-1, thromboxane A2) are crucial for clinical presentation, severity and prognosis of the disease (Sobolewski, A., et al, 2008) Dysregulation these factors via increased oxidase (NADPH oxidase family, xanthine and aldehyde oxidases) activity and bone morphogenetic protein receptor-2 signaling mechanism produce reactive oxygen species (superoxide, hydrogen peroxide, peroxynitrite) that disrupt canonic NO synthase pathway, lead to mitochondrial dysfunction and inflammation, potentiate proliferative response of the vasculature cells, mediate thickness and fibrosis of pulmonary artery vasculature The aim of the short communication is to summarize knowledge regarding the role of galectin-3 in risk stratification of PAH patients
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