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March 3, 2026Journal of Molecular and Cellular Cardiology0 citations

Tgfbr2 deficiency promotes mitochondrial dysfunction of vascular smooth muscle cells in thoracic aortic aneurysms and dissections

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ZTZhenqing TengQWQi WangYZYang Zhang

Key Points

  • Mitochondrial dysfunction is identified in vascular smooth muscle cells lacking Tgfbr2, complicating thoracic aortic aneurysms.
  • Analysis shows Tgfbr2 deficiency correlates with significant impairment in mitochondrial function—affecting smooth muscle cells.
  • The study examines thoracic aortic aneurysms and dissections induced by Tgfbr2 deficiency in animal models.
  • Highlighting the role of Tgfbr2 in smooth muscle cell function may offer new therapeutic approaches for aneurysms.
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Cite This Study

Teng et al. (2026) studied this question.

synapsesocial.com/papers/69a76191c6e9836116a2f995https://doi.org/10.1016/j.yjmcc.2026.02.004
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