![]() ![]() That, Campbell said, indicates that the stiffness of the diseased matrix itself is reprogramming active muscle contractions. In the study, the researchers observed that the tissue on the diseased matrix required twice the force to stretch to the same length as the tissue on the healthy matrix. These findings are essentially teeing up the question: How can we fix the matrix and potentially make a big difference in this disease?” “It’s almost as if the diseased matrix remembers that it was part of an unhealthy heart. “This is really surprising because these cells contain identical genetics and yet they have completely different behaviors just by virtue of which matrix they were growing on,” Campbell said. They later compared these cells with cardiac muscle cells grown on a healthy ECM and found that those grown on the diseased ECM showed prolonged contractions and poor relaxation. The heart cells were chemically removed from the tissue and replaced with healthy human heart muscle cells. Suspecting that an unhealthy ECM is the culprit, Campbell’s team first obtained diseased ECM from a pig model of HCM. Drug treatment can correct the effects of these mutations, but it doesn’t completely reverse the disease. HCM is often caused by gene mutations that affect muscle contraction. The study appears July 24 in the journal JACC: Basic to Translational Science. They found that the ECM appears to play a major role in the progression of hypertrophic cardiomyopathy (HCM), a genetic condition that causes thickened heart muscle. Stuart Campbell, associate professor of biomedical engineering & cellular and molecular physiology, led a team of researchers examined the effects of a diseased extracellular matrix (ECM) - the scaffolding material that organizes cells into tissue - on the behavior of healthy heart cells. When it comes to heart disease, the health of the scaffold where cardiac cells grow may be a much bigger factor than previously believed. ![]()
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