| First Author | Stepien DM | Year | 2020 |
| Journal | J Immunol | Volume | 204 |
| Issue | 8 | Pages | 2203-2215 |
| PubMed ID | 32161098 | Mgi Jnum | J:287172 |
| Mgi Id | MGI:6405959 | Doi | 10.4049/jimmunol.1900814 |
| Citation | Stepien DM, et al. (2020) Tuning Macrophage Phenotype to Mitigate Skeletal Muscle Fibrosis. J Immunol 204(8):2203-2215 |
| abstractText | Myeloid cells are critical to the development of fibrosis following muscle injury; however, the mechanism of their role in fibrosis formation remains unclear. In this study, we demonstrate that myeloid cell-derived TGF-beta1 signaling is increased in a profibrotic ischemia reperfusion and cardiotoxin muscle injury model. We found that myeloid-specific deletion of Tgfb1 abrogates the fibrotic response in this injury model and reduces fibro/adipogenic progenitor cell proliferation while simultaneously enhancing muscle regeneration, which is abrogated by adaptive transfer of normal macrophages. Similarly, a murine TGFBRII-Fc ligand trap administered after injury significantly reduced muscle fibrosis and improved muscle regeneration. This study ultimately demonstrates that infiltrating myeloid cell TGF-beta1 is responsible for the development of traumatic muscle fibrosis, and its blockade offers a promising therapeutic target for preventing muscle fibrosis after ischemic injury. |
