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首页> 外文期刊>American Journal of Physiology >Pretreatment with a soluble activin type IIB receptor/Fc fusion protein improves hypoxia-induced muscle dysfunction.
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Pretreatment with a soluble activin type IIB receptor/Fc fusion protein improves hypoxia-induced muscle dysfunction.

机译：用可溶性激活素IIB型受体/ Fc融合蛋白进行预处理可改善缺氧引起的肌肉功能障碍。

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Hypoxia, or reduced oxygen, occurs in a variety of clinical and environmental situations. Hypoxic exposure is associated with decreased muscle mass and a concomitant reduction in exercise capacity, although the exact mechanisms are not completely understood. The activin type IIB receptor (ActRIIB) is a receptor for transforming growth factor-beta (TGFbeta) superfamily members that are involved in the negative regulation of lean tissue mass. Given that hypoxia has negative effects on muscle mass and function and that modulation of the ActRIIB has been shown to increase muscle mass, we tested the hypothesis that pharmacological targeting of the ActRIIB for 2 wk would attenuate the loss of muscle mass and function in mice after exposure to normobaric hypoxia. ActRIIB modulation was achieved using a soluble activin receptor/Fc fusion protein (sActRIIB) in mice housed in a hypoxic chamber for 1 or 2 wk. Hypoxia induced a reduction in body weight in PBS- and sActRIIB-treated mice, although sActRIIB-treated mice remained larger throughout the hypoxic exposure. The absolute forces generated by extensor digitorum longus muscles were also significantly greater in sActRIIB- than PBS-treated mice and were more resistant to eccentric contraction-induced force drop after eccentric lengthening contractions. In summary, sActRIIB pretreatment attenuated hypoxia-induced muscle dysfunction. These data suggest that targeting the ActRIIB is an effective strategy to counter hypoxia-induced muscle dysfunction and to preacclimatize to hypoxia in clinical or high-altitude settings.
机译：缺氧或氧气减少会在各种临床和环境情况下发生。低氧暴露与肌肉质量下降和运动能力降低有关，尽管确切的机理尚不完全清楚。 IIB型激活素受体（ActRIIB）是用于转化生长因子-β（TGFbeta）超家族成员的受体，该成员参与瘦组织质量的负调控。鉴于缺氧会对肌肉质量和功能产生负面影响，并且已经证明ActRIIB的调节会增加肌肉质量，因此我们测试了以下假设：ActRIIB在2周内的药理靶向作用会减轻小鼠肌肉质量和功能的丧失暴露于常压缺氧。使用可溶性激活素受体/ Fc融合蛋白（sActRIIB）在低氧室内放置1或2周的小鼠中实现ActRIIB调节。缺氧导致PBS和sActRIIB处理的小鼠体重减轻，尽管sActRIIB处理的小鼠在整个低氧暴露中仍然较大。与PBS处理的小鼠相比，sActRIIB处理的由伸指长肌产生的绝对力也明显更大，并且对偏心收缩引起的偏心收缩引起的力下降具有更大的抵抗力。总之，sActRIIB预处理可减轻缺氧引起的肌肉功能障碍。这些数据表明，以ActRIIB为靶标是对抗缺氧引起的肌肉功能障碍并在临床或高海拔环境中预先适应缺氧的有效策略。

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