Editorial: Cardiac Fibrosis, From Lineage Tracing to Therapeutic Application

Figures

• 

  Figure 1. Cartoon depicting two pathogenic mechanisms of cardiac fibrosis, “reparative” (replacing dead cardiomyocytes) and “reactive” (interstitial and perivascular) cardiac fibrosis (blue color). Pro-fibrotic factors (TGF-β, AngII, PDGF, and CTGF) and cytokines released from inflammatory cells promote differentiation of fibroblasts toward activated myofibroblasts and matrifibrocytes actively producing extracellular matrix (ECM). Specific biomarkers of different stages of cardiac fibroblast differentiation are indicated on the bottom. TGF-β, transforming grow factor β; Ang II, angiotensin type II; PDGF, platelet derived grow factor; CTGF, connective tissue grow factor; Tcf21, transcription factor 21(biomarker for cardiac fibroblasts); Periostin, (biomarker of activated myofibroblasts) Acta2, smooth muscle actin alpha 2 (biomarker of matrifibrocytes); α-SMA, α smooth muscle actin.