![]() ![]() It explains why for years we have known statins protect people from heart attacks, even those people whose blood cholesterol levels are normal. "This finding is unique in that we found a completely new pathway to atherosclerosis. Milewicz and her team found that protein coded by this gene is not folded correctly because of the mutation, and it triggers stress in the smooth muscle cell, which then forces the cell to make more cholesterol internally, regardless of the levels of cholesterol in the blood, driving atherosclerotic plaque formation. Traditional risk factors for developing atherosclerosis include high cholesterol, high blood pressure, diabetes, smoking, obesity, lack of exercise, and consuming a high-fat diet.ĪCTA2 is typically found in the smooth muscle cells, which line the arteries and allow the arteries to contract to control blood pressure and flow. It can develop over time and most people don't know they have it until they suffer a heart attack or stroke. "It was a surprise to find that people with the gene mutation had too much atherosclerosis at a young age and with no risk factors."Ī 2009 study led by Milewicz found that a number of mutations in ACTA2 predispose humans to develop early onset (30s or younger) coronary artery disease.Ītherosclerosis is a buildup of fats, cholesterol, and other substances in and on the artery walls. "The gene ACTA2 codes a specific protein that has nothing to do with cholesterol," said Dianna Milewicz, MD, PhD, senior author of the study and professor and director of the Division of Medical Genetics at McGovern Medical School at UTHealth Houston. ![]() The study was published in the European Heart Journal. ![]()
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