Genetic lineage tracing defines myofibroblast origin and function in the injuryed heart

     Periostin-expressing myofibroblasts in the heart derive from tissue-resident fibroblasts of the TCF21 lineage, but not immune/myeloid or smooth muscle cells. Deletion of periostin+ myofibroblasts reduces collagen production and scar formation after MI. Periostin-traced myofibroblasts revert back to a less-activated state upon injury resolution.                                               

      Periostin b and collagen 1a2 expressing cells: activated fibroblast. Fibroblasts are not fully eliminated but inactivated. Unexpectedly,  blocking col1a2 expressing cells invovling fibrotic response impaired CM proliferation. Antifibrotic therapies is less efficient than inactivated fibroblast.   

 Collagen 1 was detected in endocardiaum border of injury site, but inhabition of notch signaling did not interfere the collagen deposition[R].  The effect of fibrosis on cardiomyocyte proliferation and heart regeneration is an open question[R].

1\Notch signalling restricts inflammation and serpine1 expression in the dynamic endocardium of the regenerating zebrafish heart

2\Cardiac Fibroblasts regulates CM proliferation via beta1 intergrin signaling