Madrid, 17 Mar A group of international researchers found that arteries with plaques (atherosclerotic) or abdominal aortic aneurysms (AAA) have lower levels of galectin- 1 and more galectin-1 in healthy aorta, showing that galectin-1 is an effective therapeutic target. Details of the results were published in the journal “Scientific Advancement” by the team of CIBER Cardiovascular Diseases (CIBERCV) in Spain and the National Council for Research on Science and Technology (CONICET) in Argentina. Cardiovascular disease, which can lead to myocardial infarction or stroke, is a process called atherosclerosis due to the formation of atheroma plaques in the arteries. These plaques can break and release the contents, causing clotting and the formation of blood clots that interfere with blood flow. On the other hand, the abdominal aortic aneurysm (AAA), which is characterized by the expansion of the abdominal aorta, is an asymptomatic disease that is difficult to diagnose over time and can worsen until it causes an arterial rupture. Identifying the mechanisms associated with these diseases and finding treatments to prevent mortality associated with these diseases is essential. This paper suggests that the loss of galectin-1 is associated with the development of vascular diseases. To carry out the study, the authors removed galectin from a mouse model of atherosclerosis and observed that people without this protein develop much larger plaques than those with normal levels of galectin-1. Atherosclerosis and AAA are characterized by loss of function of vascular smooth muscle cells, as well as the accumulation of cholesterol and inflammatory cells in the walls of the aorta. The study focused on the study of new mechanisms by which gallectin-1 can prevent the development of atherosclerosis and AAA, and in vitro studies, researchers found that Galectin-1 deficient macrophages present more cholesterol, but Galectin-1 treatment prevents the absorption of these cellular cholesterol. This study showed that treatment with galectin-1 in mice with atherosclerosis or AAA can prevent the development of vascular lesions through mechanisms related to muscle cell preservation. Smoothing blood vessels. “Galectin-1 treatment reduces the size of the necrotic nucleus, which is an indicator of the instability of progressive atherosclerotic plaques, preventing plaque rupture and related complications,” said José Luis Martín Ventura, of the CIBER Cardiovascular Disease Area (CIBERCV), Jiménez of the Diaz Health Institute. However, the researchers warn that more research is needed in this area. ECG/GCC
They look for proteins that prevent the development of plaques in the arteries.
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