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Stepien, David M; Hwang, Charles; Marini, Simone; Pagani, Chase A; Sorkin, Michael; Visser, Noelle D; Huber, Amanda K; Edwards, Nicole J; Loder, Shawn J; Vasquez, Kaetlin; Aguilar, Carlos A; Kumar, Ravi; Mascharak, Shamik; Longaker, Michael T; Li, Jun; Levi, Benjamin
The Journal of immunology (1950), 04/2020, Letnik: 204, Številka: 8Journal Article
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-β1 signaling is increased in a profibrotic ischemia reperfusion and cardiotoxin muscle injury model. We found that myeloid-specific deletion of 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-β1 is responsible for the development of traumatic muscle fibrosis, and its blockade offers a promising therapeutic target for preventing muscle fibrosis after ischemic injury.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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