Soluble activin receptor type IIB-mediated inhibition improves muscle regeneration following Crotalus atrox venom-induced damage

Sonavane, M., Alqallaf, A., Mitchell, R. D., Almeida, J. R., Gilabadi, S., Richards, N. J., Adeyemi, S., Williams, J., Ritvos, O., Vaiyapuri, S. ORCID: https://orcid.org/0000-0002-6006-6517 and Patel, K. (2025) Soluble activin receptor type IIB-mediated inhibition improves muscle regeneration following Crotalus atrox venom-induced damage. Toxins, 17 (2). 59. ISSN 2072-6651 doi: 10.3390/toxins17020059

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.

Item Type	Article
URI	https://reading-clone.eprints-hosting.org/id/eprint/120375
Item Type	Article
Refereed	Yes
Divisions	Life Sciences > School of Biological Sciences > Biomedical Sciences Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy > Division of Pharmacology
Publisher	MDPI
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