According to a study that points to a new strategy for preventing or possibly reversing fibrosis, the scarring that can lead to organ and tissue damage, a molecule called Epac (Exchange protein activated by cAMP1), plays a key role in integrating the body’s pro-fibrotic and anti-fibrotic response. Cardiac fibrosis can result in a decline in cardiovascular function that occurs with aging or, in some patients, after a heart attack. The study, conducted by a group of researchers led by Paul A. Insel, indicated that increasing Epac expression inhibited the synthesis of collagen, which promotes tissue fibrosis.