High levels of a protein called galectin-3 are associated with pulmonary hypertension deaths, according to a study that says targeting the protein could be a way to develop treatments for PH.
In fact, the higher the level of the protein, the higher the death rate, the research showed.
The study, “Galectin-3 Levels Are Elevated and Predictive of Mortality in Pulmonary Hypertension,” was published in the journal Heart, Lung and Circulation.
PH is characterized by high blood pressure in lung vessels. One of the two forms that were part of the galactin-3 study was pulmonary arterial hypertension (PAH), where high blood pressure occurs in arteries that supply blood to the lungs.
The other PH form studied was one associated with a condition known as heart failure with preserved ejection fraction (HFpEF-PH). The heart’s inability to function properly under that condition causes high blood pressure in lung vessels, as opposed to arteries.
Galectin-3 is a naturally occurring substance produced by a type of white blood cell called a macrophage. It is involved in inflammation and fibrosis, or the thickening and scarring of connective tissue. Connective tissue binds other tissues together.
The study included 76 patients, 37 with PAH and 39 with HFpEF-PH. Blood was collected from a lung artery using right heart catheterization (RHC). That involved threading a narrow tube through an artery in the neck to a lung artery.
Galectin-3 levels were measured in the blood samples. Researchers used the measurements to divide the patients into three groups: those with lower levels — 25 patients; mid-range levels — 26 patients; and higher levels — 25 patients.
The death rate in the group with lower galectin-3 levels was 16.7%. It was 30.4% in the mid-range group, and 52.2% in the high-range group. The figures showed that the higher the galectin-3 level, the higher the patient mortality rate.
“Our study demonstrates that galectin-3 is significantly elevated in PH, regardless of aetiology [the cause], and is independently predictive of mortality. Future studies are needed to further clarify the origin of fibrosis as indicated by elevated galectin-3 levels, especially in PAH, as well as assess the role of galectin-3 as a biomarker and therapeutic target to identify those who may benefit from PH-specific therapy, in both PAH and HFpEF-PH,” the team concluded.
Th researchers cautioned that the study “measured galectin-3 at an initial time-point. It, therefore, does not address the causal role of galectin-3 in the development of PAH or HFpEF-PH.”