Coronary artery disease (CAD) is the most common type of heart disease in the United States. It is sometimes called coronary heart disease or ischemic heart disease. CAD is caused by plaque buildup in the walls of the arteries that supply blood to the heart (called coronary arteries) and other parts of the body. Plaque is made up of deposits of cholesterol and other substances in the artery. Plaque buildup causes the inside of the arteries to narrow over time, which can partially or totally block the blood flow. This process is called atherosclerosis. Now there might be radical help for this condition.
Michigan State University and Stanford University scientists have invented a radical treatment, which, if it clears further tests, can help people suffering from the condition. A new nanoparticle eats away -- from the inside out -- portions of plaques that cause heart attacks. The nanoparticle that can be directed with high selectivity to a particular immune cell type -- monocytes and macrophages. Once inside the macrophages in those plaques, it delivers a drug agent that stimulates the cell to engulf and eat cellular debris. Basically, it removes the diseased/dead cells in the plaque core. By reinvigorating the macrophages, plaque size is reduced and stabilized. It is highly expected that the treatment would reduce the risk of most types of heart attacks, and it would have minimal side effects.
Small molecules using nano-immunotherapeutic platforms could stimulate the macrophages to selectively eat dead and dying cells, the precursor cells to atherosclerosis. Delivering a small molecule inside the macrophages has an enormous advantage. The next step will be to start a clinical translation of these nanomaterials using large animal models and human tissue tests.
The discovery could be a potential treatment for atherosclerosis, a leading cause of death in many parts of the world.
Read more:
Nature Nanotechnology: Nanoparticles are specifically taken up by lesional macrophages to prevent atherosclerosis.
Copyright © 2020 by Eva Deli
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