Galectin-3 (Gal-3) and the hormone aldosterone are two potential biomarkers for disease progression in patients with pulmonary arterial hypertension, according to a recent study, “Galectin-3 and aldosterone as potential tandem biomarkers in pulmonary arterial hypertension,” published in the journal Heart.
Aldosterone, a steroid hormone that is responsible for regulating the salt and water balance in the body, was previously suggested to have a role in pulmonary vascular remodeling and fibrosis. Notably, increased levels of aldosterone were also found in tissues and blood of people with pulmonary arterial hypertension.
The mechanisms of action of aldosterone and its effects in the cardiovascular system were suggested to occur via Gal-3, a β-galactoside-binding lectin with established roles in inflammation, fibrosis, and heart failure.
Because clinical studies on the role of both Gal-3 and aldosterone in pulmonary arterial hypertension are lacking, a team of researchers investigated the link between aldosterone/Gal-3, and their association with disease severity. They analyzed 57 patients, 41 with idiopathic pulmonary arterial hypertension and 16 with pulmonary arterial hypertension associated with connective tissue disease, and healthy controls (in total, eight matched for age with pulmonary arterial hypertension patients). The researchers measured, in both pulmonary arterial hypertension patients and controls blood samples, the levels of Gal-3, aldosterone, and other plasma proteins.
They found that patients with idiopathic pulmonary arterial hypertension and pulmonary arterial hypertension-connective tissue disease had increased levels of Gal-3 values (12.2 ng/mL and 14.1 ng/mL, respectively) when compared to controls (8.5 ng/mL); aldosterone levels were increased in patients with idiopathic pulmonary arterial hypertension only (248.5 pg/mL versus 71.9 pg/mL in controls). Moreover, aldosterone and Gal-3 levels (but also N-terminal pro-brain natriuretic peptide, NT-proBNP) had higher levels in pulmonary arterial hypertension patients in more advanced stages of the disease (WHO functional class II–III) then those in earlier stages (WHO functional class I) or controls.
In conclusion, the higher concentration of Gal-3 and aldosterone in blood samples of pulmonary arterial hypertension patients suggest that the Gal-3 mediate pathway is important for disease progression. These molecules may serve as potential biomarkers of disease severity.
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