| First Author | Nawaz A | Year | 2022 |
| Journal | Nat Commun | Volume | 13 |
| Issue | 1 | Pages | 7058 |
| PubMed ID | 36411280 | Mgi Jnum | J:332989 |
| Mgi Id | MGI:7410292 | Doi | 10.1038/s41467-022-34191-y |
| Citation | Nawaz A, et al. (2022) Depletion of CD206(+) M2-like macrophages induces fibro-adipogenic progenitors activation and muscle regeneration. Nat Commun 13(1):7058 |
| abstractText | Muscle regeneration requires the coordination of muscle stem cells, mesenchymal fibro-adipogenic progenitors (FAPs), and macrophages. How macrophages regulate the paracrine secretion of FAPs during the recovery process remains elusive. Herein, we systemically investigated the communication between CD206(+) M2-like macrophages and FAPs during the recovery process using a transgenic mouse model. Depletion of CD206(+) M2-like macrophages or deletion of CD206(+) M2-like macrophages-specific TGF-beta1 gene induces myogenesis and muscle regeneration. We show that depletion of CD206(+) M2-like macrophages activates FAPs and activated FAPs secrete follistatin, a promyogenic factor, thereby boosting the recovery process. Conversely, deletion of the FAP-specific follistatin gene results in impaired muscle stem cell function, enhanced fibrosis, and delayed muscle regeneration. Mechanistically, CD206(+) M2-like macrophages inhibit the secretion of FAP-derived follistatin via TGF-beta signaling. Here we show that CD206(+) M2-like macrophages constitute a microenvironment for FAPs and may regulate the myogenic potential of muscle stem/satellite cells. |
