They produce peptides that prevent LDL cholesterol from aggregating.
Researchers from the Barcelona Institute of Biomedical Research (IIBB-CSIC) and the Sant Pau Research Institute (IR Sant Pau), led by Dr. Vicenta Llorente Cortes, together with the CIBER groups on Cardiovascular Diseases (CIBERCV) and Diabetes and Related Metabolic Diseases (CIBERDEM) have developed peptides that inhibit the aggregation of LDL cholesterol (abbreviation in English language, denoting lipoproteins). low density), which prevent the formation of atherosclerotic plaques, in an experimental model of hypercholesterolemia.
A study that was just published in magazine Atherosclerosis, Also participating are teams from the Miguel Servet Hospital in Zaragoza and the University of Basilicata in Italy. Atherosclerosis, the leading cause of heart attacks and strokes, is caused by the buildup of LDL cholesterol in the blood in the walls of the arteries.
LDL accumulated in the wall changes, promoting the progression of plaques, which can rupture and block normal circulation, causing blood clots to form, causing acute myocardial infarction.
These new peptides currently developed represent a promising and novel advance in the treatment of this disease. Its potential is particularly relevant for patients with a genetic predisposition to atherosclerosis, such as familial hypercholesterolemia, for whom current therapeutic options are limited and its effectiveness in suppressing this disease is insufficient to reduce cardiovascular risk, which makes the search for new solutions urgent.
Prevent plaque formation
As explained Llorente Corteswho heads the Lipids and Cardiovascular Research Group at IIBB-CSIC, “In this study, we have developed peptides that bind and stabilize the structure of LDL particles. “In addition, in a humanized mouse model of lipoproteins, we showed that administration of these peptides inhibits atherosclerosis while maintaining the structural integrity of LDL.”
This effect, Llorente explains, is achieved by stabilizing the conformation of ApoB100, a protein found in LDL particles and essential for maintaining their integrity and preventing them from being modified in the arteries. Likewise, “we show the effectiveness of this treatment on LDL cholesterol samples isolated from patients with familial hypercholesterolemia.”
The relevance of this innovative treatment method lies in its unique ability to stabilize the structure of ApoB100 and maintain the integrity of LDL particles in the vascular wall, preventing their aggregation – a key process in the development of atherosclerosis.
Help Article:
Benitez-Amaro, A., Garcia, E., La Chica Lest, M. T., Martinez, A., Borras, C., Tondo, M., … Llorente-Cortes, V. (2024). Targeting LDL aggregation reduces atherosclerotic lipid load in a humanized mouse model of familial hypercholesterolemia: critical role of conformational stabilization of ApoB100. Atherosclerosis(118630), 118630. doi:10.1016/j.atherosclerosis.2024.118630