Report discovers root of cardiac fibrosis

A report published in Nature Medicine by researchers at Beth Israel Deaconess Medical Center (BIDMC) helps explain the roots of cardiac fibrosis. The research further showed that the bone morphogenic molecule known as rhBMP7 might prove to be a therapy for cardiac fibrosis. The study used mice, in which endothelial cells had been marked genetically, to confirm the conversion of cells into fibroblasts during cardiac fibrosis. These cells were responsible for slowing down the proper function and electrical conduction of the heart. In the second part of the study, the investigators analyzed the rhBMP7 protein to determine its function in reducing the development of fibroblasts. “These findings provide compelling proof that the process of fibrosis can be reversed in the heart and offers the possibility of new therapies for patients who have developed cardiac fibrosis as the result of myocardial infarction, hypertension, valvular diseases or heart transplantation,” said senior author of the study, Dr. Raghu Kalluri.

Researchers from the University of Edinburgh found that heart disease might lead to a decline in cognitive function. The four-year study evaluated 452 elderly individuals who were suffering from at least one type of cardiovascular disease. The results showed that individuals who had suffered from multiple strokes during the trial period experienced a decline in verbal memory performance. But, researchers also found that atherosclerosis reduces the flow of blood required to feed the brain and hence gradually degrades the cognitive function of individuals. “Anything that leads to better cardiovascular health – more favorable levels of cardiovascular risk factors, blood pressure, cholesterol, not to smoke – these are all likely to impact the brain, the blood flow to the brain, arterial function, and eventually cognitive function,” said lead researcher, Dr. Snorri Bjorn Rafnsson.

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