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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：用可溶性活素型IIB受体/ Fc融合蛋白的预处理改善了缺氧诱导的肌肉功能障碍。

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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：缺氧或减少的氧气，发生在各种临床和环境情况下。缺氧暴露与肌肉质量下降和运动能力的伴随减少相关，尽管未完全理解确切的机制。活素型IIB受体（ActRIIB）是用于转化涉及贫组织物质的负调节的生长因子-β（TGFBETA）超家族成员的受体。鉴于缺氧对肌肉质量和功能产生负面影响并且已经显示出肌肉的调节增加肌肉质量，我们测试了Actriib的药理靶向2周的药理靶向会衰减后的肌肉质量损失和小鼠的功能接触正常缺氧。使用在缺氧室内的小鼠中使用可溶性活素受体/ Fc融合蛋白（Sactriib）来实现ActRIIB调节，以1或2WK。缺氧诱导在PBS和Sactriib处理的小鼠中减少体重，尽管在整个缺氧暴露过程中保持较大。在偏心延长收缩后，延伸位二维肌腱产生的绝对力在骶髂肿瘤中也显着大于PBS处理的小鼠并且更耐偏心收缩诱导的力下降。总之，Sactriib预处理减弱了缺氧诱导的肌肉功能障碍。这些数据表明，靶向Actrib是对缺氧诱导的肌肉功能障碍并在临床或高空环境中进行缺氧的有效策略。

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