Abstract
Pulmonary arterial hypertension (PAH) is a heterogenic group of devastating disorders that characterizes higher rates of mortality and morbidity worldwide. Recent clinical studies have shown that clinical features, hemodynamic parameters, echocardiography patter, multi-spiral computer tomography findings, exercise capacity, and anti-nuclear antibody profiles could be used as predictors of clinical severity and outcomes in PAH patients. However, the reliability, sensitivity, specificity and predictive value are derived from PAH patients with different comorbidities and specific complications associated with connective tissue disease (CTD), congenital heart disease and respiratory disease might be unacceptable. The aim of the mini review: to summarize the knowledge regarding predictive value of galectin-3 as a biomarker in PAH individuals. The mini review is argued the perspective to utilize single sample and serial measurements of Gal-3 as a regulatory peptide contributed in PAH pathogenesis aimed to improve prediction of PAH development and progression.
Highlights
Pulmonary arterial hypertension (PAH) is a heterogenic group of distinct disorders that includes idiopathic PAH (IPAH), familial PAH and PAH associated with other conditions (APAH) such as connective tissue disease (CTD-APAH), respiratory disease, congenital or acquired left-heart inflow/outflow obstructive lesions or congenital cardiomyopathies etc. [1,2]
Despite histological findings that are suitable for the pulmonary vascular lesions in PAH complicating CTD are similar to those observed in IPAH, familial PAH and APAH, morbidity and mortality rates between these patient cohorts sufficiently distinguish
Compared with IPAH patients and familial PAH individuals, patients with PAH associated with CTD have an older age of onset and exhibited worse prognosis in survival
Summary
Pulmonary arterial hypertension (PAH) is a heterogenic group of distinct disorders that includes idiopathic PAH (IPAH), familial PAH and PAH associated with other conditions (APAH) such as connective tissue disease (CTD-APAH), respiratory disease, congenital or acquired left-heart inflow/outflow obstructive lesions or congenital cardiomyopathies etc. [1,2]. Recent pre-clinical and clinical studies have been indicated an important role for Gal-3 signaling mechanism in the pathophysiology of IPAH and PAH-CTD [15,16]. Gal-3 acts a fundamental regulator of inflammation, fibrosis, angiogenesis, adhesion, tumor growth and progression, and immunological functions [17,18,19].
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call