The extracellular matrix (ECM) is increasingly being recognized as a dynamic network of molecules that participates actively in the cellular signaling events that determine an organ's state of health. Most forms of heart failure, for example, are accompanied by alterations in the composition of the ECM. Myocardial infarction (MI) leads to a dramatic increase in the expression of periostin, a 90-kD protein secreted by fibroblasts, yet whether periostin promotes repair of heart damage or contributes to it has been unclear. The answer may be both, as indicated by two research groups who have independently explored periostin function using distinct model systems. In a cell culture study, Kühn et al. found that the addition of recombinant periostin to differentiated rat cardiomyocytes caused them to reenter the cell cycle and divide, a process that required integrins as well as phosphatidylinositol 3-kinase. Sustained delivery of recombinant periostin to the heart of rats after experimental MI reduced the extent of heart damage and improved heart function, leading the authors to conclude that the protein enhances heart repair. Oka et al. studied mice genetically deficient in periostin. Intriguingly, the mutant mice showed improved cardiac function after MI over the long term, a result the authors attribute to the protein's role in regulating cardiac remodeling and hypertrophy. — PAK
Nat. Med. 13, 10.1038/nm1619 (2007); Circ. Res. 10.1161/CIRCRESAHA.107.149047 (2007).