Gal-3+ Macrophages and Osteopontin are upregulated in skeletal muscle fibrosis

A group from Department of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA, etc. has reported about an unique macrophage population associated with skeletal muscle fibrosis.

Macrophages have a central role in innate immunity and contribute to tissue homeostasis by regulating tissue repair and remodeling of the extracellular matrix. There are two types of macrophagese, M1 and M2. In acute muscle trauma, proinflammatory M1 macrophages initially infiltrate injured muscle to phagocytose cellular debris and activate muscle stem cells. The subsequent transition to M2 macrophages in the regenerative phase promotes muscle stem cell differentiation and the resolution of inflammation.

In the case of skelectal muscle fibrosis, it was found that gal-3+ macrophages are are chronically activated during muscular dystrophy. Spatial transcriptomic analysis of dystrophic muscle revealed that areas enriched in gal-3+ macrophages and stromal cells expressed genes associated with muscle fibrosis. Furthermore, gal-3+ macrophages colocalize with stromal cells in dystrophic lesions, and osteopontin (Spp1) mediates communication between these cell types.