In a study that points to a new strategy for preventing or possibly reversing fibrosis the scarring that can lead to organ and tissue damage researchers at the University of California, San Diego School of Medicine have determined that a molecule called Epac (Exchange protein activated by cAMP1), plays a key role in integrating the bodys pro- and anti-fibrotic response. The research will be published in the online edition of the Proceedings of the National Academy of Science (PNAS) the week of April 21.
Inflammation is the bodys response to injury in tissues, prompting healing that leads to scars, whether on the skin, or in organs such as the heart, liver or lungs. Such scarring has beneficial properties, but theres also the risk of excessive scarring, or tissue fibrosis, that can lead to organ damage and loss of function.
The UC San Diego researchers looked at cardiac fibrosis, which can occur in patients who have suffered an infection of the heart muscle or a heart attack. Such fibrosis causes the heart to stiffen so that it cannot adequately fill with blood and then empty itself, a condition known as diastolic dysfunction.
An old heart is a stiff heart and some injured hearts are stiff as well, said Paul A. Insel, M.D., UCSD professor of pharmacology and medicine, and principal investigator of the study. Much of the decrease in cardiovascular function that occurs with aging or, in some patients after a heart attack, can be explained by fibrosis. We wondered: What is responsible for excessive fibrosis" Is there a way to decrease or possibly reverse it"
It was previously known that a messenger molecule inside of cells, called cAMP, can block fibrosis in the heart. Insel and colleagues explored the mechanism leading to the anti-fibrotic effect, and discovered that the Epac molecule mediates cAMP actions that are involved in cardiac fibrosis. Epac also helps regulate other proteins that contribute to cell death, di
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University of California - San Diego