Myofibroblast Forms Atherosclerotic Plaques

For many years, scientists believed that atherosclerotic plaques—the dangerous buildups that clog arteries and lead to heart attacks—were primarily formed by two types of cells: smooth muscle cells and immune cells called macrophages. However, this new research from Chinese cardiovascular scientists challenges that long-held belief by examining actual human coronary artery plaques under the microscope.

The researchers made a surprising discovery: instead of finding many smooth muscle cells in the plaques, they found that specialized cells called myofibroblasts were the dominant players. These myofibroblasts appeared to be responsible for creating the fibrous cap (the outer layer of plaques), producing collagen fibers that strengthen the plaque structure, and even transforming into foam cells—the cholesterol-laden cells that are a hallmark of atherosclerosis. The distribution of these myofibroblasts directly correlated with how thick the artery walls had become.

To confirm their findings, the research team recreated plaque formation in laboratory conditions using human myofibroblasts. Remarkably, these cells were able to take up LDL cholesterol (the "bad" cholesterol) and spontaneously form structures that closely resembled real atherosclerotic plaques, complete with foam cells, excess lipids, and collagen fibers. This was the first time scientists had successfully created such realistic plaque models in the lab using a single cell type.

This discovery could significantly simplify our understanding of how heart disease develops and potentially lead to more targeted treatments. Rather than viewing atherosclerosis as a complex process involving multiple cell types, it may primarily be the result of myofibroblasts responding to vascular injury from risk factors like high cholesterol, high blood sugar, or inflammation. For patients focused on metabolic health and longevity, this research reinforces the importance of controlling traditional cardiovascular risk factors, as these appear to trigger the myofibroblast remodeling process that builds dangerous plaques. While this is preliminary research that requires peer review and clinical validation, it may eventually lead to new therapeutic approaches targeting these specific cells.