Abstract/Summary

Viper bite envenomation often results in prominent skeletal muscle damage. According to our previous studies, prolonged pres-ence of C. atrox venom toxins induced extensive muscle damage which mimicked the outcome of chronic muscle damage often seen in human muscular dystrophies. In the case of chronic muscle damage, two critical processes occur: muscle regeneration is im-paired, and fibrosis develops. Myostatin/Activin signalling is a key regulator of both of these processes. Myostatin and its closely related molecules in particular Activin inhibit myocyte proliferation and differentiation while promoting fibroblast proliferation and expression of extracellular matrix proteins. Thus, attenuating Myostatin/Activin signalling offers an attractive means of promoting muscle development while decreasing fibrosis. Hence, we have used the soluble Activin Receptor type IIb, which acts as a ligand trap for both Myostatin and Activin to dampen signalling and assessed whether this intervention can alter the patholog-ical trajectory of C. atrox venom-induced muscle damage in mice. We report that the soluble Activin Receptor type IIb treatment increased the size of regenerating fibres while at the same time reducing the level of fibrotic tissue in muscle damaged with C. atrox venom.