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The YAP/TAZ-Tgfbr2-stiffness feedback loop governs divergent cell fates of muscle-resident mesenchymal progenitors.
Cell Reports · · Journal Article
Iwamori, Horikiri + more
Abstract ↗AI summary
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Interstitial stiffness linked to YAP/TAZ activity governs muscle-resident mesenchymal progenitor fate, with YAP/TAZ deficiency enhancing fat deposition in the fat accumulation model.
- Why it matters: Muscle-resident mesenchymal progenitors can regenerate tissue or contribute to fat and fibrosis, but how stiffness and mechanotransduction cues are integrated to choose fate is unclear.
- What they did: The study compared fat accumulation versus regeneration models by measuring interstitial stiffness and nuclear YAP/TAZ-positive progenitors, then tested YAP/TAZ and Tgfbr2 loss in mesenchymal progenitors.
- The result: YAP/TAZ induced Aldh1a2 and Wnt5a and the pro-fibrogenic Tgfbr2, and Tgfbr2 loss reduced transient collagen deposition, decreased stiffness, and increased fat accumulation during regeneration.
The findingWhy it mattersWhat they didThe result
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