Less scarring for broken hearts

A process that controls excessive formation of scar tissue following a heart attack is described online in Nature Cell Biology this week. Preventing this process allows for improved recovery of heart function post injury.

Myocardial infarction, commonly known as heart attack, is responsible for 13% of deaths worldwide and is a leading cause of death in developed countries. Thomas Sato and co-workers studied a mouse gene encoding the protein sFRP2, which negatively regulates the activity of an enzyme crucial for frog and fish embryonic development. They find that in mice, sFRP2 enhances the activity of the same enzyme in breaking down a precursor of collagen, the main component deposited in scar tissue. Collagen formation is dependent on the breakdown of this precursor protein during excessive formation of scar tissue, which is known to impair recovery of heart function. Thus, sFRP2 normally enhances collagen deposition in the scar tissue and prevents heart recovery.

The authors show that mice that do not carry the Sfrp2 gene have less scar tissue than normal mice after an injury that restricts blood flow through the heart. These mice have an improved recovery of their heart function, suggesting that inhibiting sFRP2 may be an effective approach to controlling excessive scarring and improving cardiac function after myocardial infarction.