論文 - 詳細
| RRC ID | 73086 |
|---|---|
| 著者 | Nawaz A, Bilal M, Fujisaka S, Kado T, Aslam MR, Ahmed S, Okabe K, Igarashi Y, Watanabe Y, Kuwano T, Tsuneyama K, Nishimura A, Nishida Y, Yamamoto S, Sasahara M, Imura J, Mori H, Matzuk MM, Kudo F, Manabe I, Uezumi A, Nakagawa T, Oishi Y, Tobe K. |
| タイトル | Depletion of CD206+ M2-like macrophages induces fibro-adipogenic progenitors activation and muscle regeneration. |
| ジャーナル | Nat Commun |
| Abstract |
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-β1 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-β 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. |
| 巻・号 | 13(1) |
| ページ | 7058 |
| 公開日 | 2022-11-21 |
| DOI | 10.1038/s41467-022-34191-y |
| PII | 10.1038/s41467-022-34191-y |
| PMID | 36411280 |
| PMC | PMC9678897 |
| MeSH | Adipogenesis* Animals Follistatin* Macrophages Mannose Receptor / immunology Mice Mice, Transgenic Muscles |
| IF | 12.121 |
| オルトメトリクス指標 |
オルトメトリクス指標項目
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| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 23 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| 実験動物マウス | RBRC09616 |