Understanding the Process of Fibrosis in Duchenne Muscular Dystrophy

Figure 1

Crosstalk between TGFβ signaling and the renin-angiotensin system in fibrosis. TGFβ can signal via its canonical pathway, involving Smad proteins, or through several alternative pathways such as the p38 MAPK signaling or the RAS/ERK MAPK signaling pathways. Both canonical and alternative pathways lead to expression of molecules implicated in fibrosis such as CTGF or PAI-1. Similarly, Ang II signals through AT1 or AT2 and can also activate Smad proteins and the p38 MAPK signaling pathway, leading to increased expression of profibrotic genes. Ang 1–7 has an opposite effect, inhibiting the canonical TGFβ pathway. Antifibrotic molecules inhibiting RAS or the TGFβ signaling are indicated in red.