![]() ![]() His research team found ADAM17 highly expressed in fat and even higher in the blood vessels of aged human fat. The bottom line: the walls of the hair-sized microvasculature become thicker, less elastic, less able to dilate and to properly sustain the heart. The MCG scientist found that ADAM17 cleaves TNF from fat, releasing it into the bloodstream where it preferentially targets the heart. TNF is a multifunctional protein, or cytokine, that gets its name from its skill at killing tumors and is a major promoter of inflammation that also directly impacts the function of the endothelial cells that line blood vessels. In patients and animal models, who are both older and obese, Bagi has found a key dynamic in the dysfunction is an enzyme called ADAM17, which is involved in a huge variety of functions like releasing growth factors as we develop, but also implicated in diseases from Alzheimer’s to arthritis.ĪDAM17 levels increase in obesity while levels of its natural inhibitor, the protein caveolin-1, decrease with age, enabling the perfect storm.ĪDAM17 was discovered 20 years ago for its ability to cut and release previously inactive tumor necrosis factor, or TNF, from the cell membrane. What isn’t readily seen with these routine exams is the thickened walls that can hinder dilation of the small capillaries fed by these bigger vessels, a condition called coronary microvascular dysfunction, or cardiac syndrome X, says Bagi, corresponding author of the study in the journal Arteriosclerosis, Thrombosis, and Vascular Biology. ![]() “They have normal large blood vessels in the heart still the heart failure has developed.” Zsolt Bagi, vascular biologist in the Vascular Biology Center at the Medical College of Georgia at Augusta University. “Older obese patients and sometimes women who suffer heart failure go to the cardiac catheterization lab and the cardiologist finds nothing that would explain their heart failure,” said Dr. They call it “aged fat” and scientists now have evidence that the inflammation created by both age and fat have an additive effect that can thicken the walls of our coronary microvasculature without any evidence of the classic atherosclerotic plaque that many of us associate with heart disease. Age and obesity appear to create a perfect storm that can reduce blood flow through the tiny blood vessels that directly feed our heart muscle and put us at risk for heart failure, scientists report. ![]()
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