Old hearts are Fibrotic Hearts.

A heart infection or a heart attack in the past can also cause fibrosis of the heart (a build over of scare tissue at the site of the repaired injury). Science Daily, April 23, 2008, reported that University of California, San Diego, researchers determined a molecule called Epac (Exchange protein activated by cAMP1), is important in the fibrotic response. By increasing Epac expression, they were able to block the ability of agents to promote fibrosis, that is, inhibit the synthesis of collagen.

ScienceDaily, Sep. 24, 2008, reported that The University of Western Ontario also studied the mechanisms involved in fibrotic diseases, as well as a way to control it. According to the article in ScienceDaily, online, a protein called glycogen synthase kinase 3 acts as a brake to stop further repair to damaged tissue. If this protein is impaired, the repair process continues on and scarring results after wounding. They also discovered elevated levels of another protein called endothelin-1 that, if they blocked it, prevented scarring.

More recently, ScienceDaily, Feb 26, 2009, reports on a research published by Cell Press that platelet derived growth factors (PDGF) are activated by antibodies that attract PDGFR, (PDGF plus receptor alpha), when fibroblasts proliferate and deposit excessive connective tissue, leading to progressive scarring. They discovered that signaling takes place through an Ink4a/Arf-dependent mechanism. They are now looking at ways of blocking PDGFR.

Let's hope they soon come up with a pill that will undo fibrotic tissue.