After vascular injury, repair is restricted in the presence of FSAP (right) to prevent narrowing of the blood vessel.

Approximately 5% of the population carries an FSAP polymorphism linked to cardiovascular disease. The authors' previous in vitro evidence suggested that wild-type FSAP, a plasma protein, limits vessel repair processes in part by inactivating PDGF-BB—a growth factor which promotes the proliferation and migration of blood vessel wall cells during repair.

The team isolated and characterized the mutated form of FSAP and discovered that although its ability to bind PDGF-BB was unaltered, it failed to cleave the protein efficiently. Wild-type human FSAP reduced vascular cell proliferation and accumulation at sites of injury in a mouse model—most likely by reducing PDGF-BB activity. The mutant protein, however, provided no such restraint, suggesting that people possessing the mutation might generate excessive scar tissue during vessel repair.

Vessel narrowing occasionally recurs after surgical repair. If, as the team suspects, recurrence correlates with the FSAP polymorphism, then screening cardiovascular patients for the mutation might identify those at risk.