Key points from article :
A groundbreaking study led by Dr. Vicenta Llorente-Cortés, group leader at CSIC, and published in the Journal of Lipid Research has uncovered how cholesterol damages the heart at a cellular level—and introduced a promising new treatment to reverse the harm. The international research team found that cholesteryl esters, carried by lipoproteins in the blood, can infiltrate cardiomyocytes (heart muscle cells) and accumulate inside their mitochondria, the cell’s energy factories. This build-up disrupts mitochondrial structure and function, significantly impairing the heart’s ability to produce energy.
At the core of this mechanism is the LRP1 receptor, which transports cholesterol into the cells. Under conditions like obesity or high cholesterol, this process becomes harmful, leading to mitochondrial dysfunction—a contributor to heart failure. To combat this, the researchers developed an experimental immunotherapy using monoclonal antibodies that block the LRP1 receptor, preventing the harmful transport of cholesterol into the heart’s mitochondria.
Using advanced imaging and bioenergetic tools, along with a rabbit model that mimics human cholesterol profiles, the team demonstrated that this treatment not only reduces mitochondrial cholesterol build-up but also restores energy production and cellular structure. Notably, the therapy improved ATP production and normalized interactions between mitochondria and lipid stores inside cells—suggesting a deeper metabolic recovery.
This innovative approach offers a new therapeutic strategy for cardiovascular diseases where cholesterol plays a damaging intracellular role, such as in diabetes, obesity, and chronic hypercholesterolemia. Rather than just lowering cholesterol levels in the blood, this treatment tackles the problem inside the cell, offering hope for more effective protection of heart health in high-risk patients.
