The slow-release adiponectin analog ALY688-SR modifies early-stage disease development in the D2.<i>mdx</i> mouse model of Duchenne muscular dystrophy
Catherine A. Bellissimo, Shivam Gandhi, L Castellani, Mayoorey Murugathasan, Luca J. Delfinis, Arshdeep K. Thuhan, Madison C. Garibotti, Yeji Seo, Irena A. Rebalka, Henry H. Hsu, Gary Sweeney, Thomas J. Hawke, Ali A. Abdul‐Sater, Christopher G. R. Perry
Abstract
There are limited therapies for the treatment of Duchenne muscular dystrophy. As fibrosis involves an accumulation of collagen that replaces muscle fibers, antifibrotics may help preserve muscle function. We report that the novel adiponectin receptor agonist ALY688-SR prevents fibrosis in the diaphragm of D2. mdx mice with short-term treatment early in disease progression. These responses were related to altered inflammation and mitochondrial functions and serve as a foundation for the development of this class of therapy.