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  1. 原著論文

Calcitonin receptor downregulation and exercise-conditioned blood enable systemic muscle stem cell proliferation

https://repo.qst.go.jp/records/2003004
https://repo.qst.go.jp/records/2003004
0d74820d-9f9f-4a26-8ca0-81c537e71c58
アイテムタイプ 学術雑誌論文 / Journal Article(1)
公開日 2026-03-12
タイトル
タイトル Calcitonin receptor downregulation and exercise-conditioned blood enable systemic muscle stem cell proliferation
言語 en
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
著者 Lidan Zhang

× Lidan Zhang

Lidan Zhang

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Takayuki Kaji

× Takayuki Kaji

Takayuki Kaji

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Ayasa Nakamura

× Ayasa Nakamura

Ayasa Nakamura

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Nagomu Maesawa

× Nagomu Maesawa

Nagomu Maesawa

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Kanako Iwamori

× Kanako Iwamori

Kanako Iwamori

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Jiayao Xu

× Jiayao Xu

Jiayao Xu

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Akiyoshi Uezumi

× Akiyoshi Uezumi

Akiyoshi Uezumi

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Daisuke Kamimura

× Daisuke Kamimura

Daisuke Kamimura

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Murakami Masaaki

× Murakami Masaaki

Murakami Masaaki

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Werner Muller

× Werner Muller

Werner Muller

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Atsushi Kubo

× Atsushi Kubo

Atsushi Kubo

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Takayuki Akimoto

× Takayuki Akimoto

Takayuki Akimoto

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So-ichiro Fukada

× So-ichiro Fukada

So-ichiro Fukada

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抄録
内容記述タイプ Abstract
内容記述 Quiescent muscle stem cells (MuSCs) respond to exercise; however, the coordinated regulation of increased loading, exerkines, and quiescence signaling remains unclear. We found that increased loading reduces calcitonin receptor (CalcR) expression, and forced activation of protein kinase A (PKA), a downstream of CalcR signaling, suppresses MuSC proliferation. Although MuSC-specific Calcr knockout (C-cKO) alone is insufficient, exercised C-cKO mice exhibit significant MuSC proliferation independent of increased loading. Reinforcement of CalcR signaling, either through PKA induction or Yap1 depletion, suppresses MuSC proliferation. Load-independent MuSC proliferation is also suppressed by the deletion of gp130 in C-cKO mice. Serum from exercised mice recapitulates MuSC proliferation in all analyzed muscles of sedentary C-cKO mice, which is abrogated by anti-IL-6 antibodies, and we find cross-talk between CalcR and gp130 signaling via Yap1 phosphorylation. Together, our findings reveal an integrated mechanism by which increased loading, exerkine-gp130, and CalcR signaling converge to fine-tune MuSC activity during exercise.
書誌情報 Nature Communications (Online Only URL:http://www.nature.com/ncomms/index.html)

巻 16, 号 1, p. 10576, 発行日 2025-11
ISSN
収録物識別子タイプ ISSN
収録物識別子 2041-1723
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Ver.1 2026-04-06 05:23:34.963336
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