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Circ Res：科学家发现可导致心衰患者肌肉损耗的信号通路

2015-08-13 sunshine 译 MedSci原创

肌肉损失心衰信号通路RAAS血管紧张素II
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发达国家心肌功能不全的患者通常会伴有肌肉损失和肌肉力量的下降。事实上直到现在，消极影响疾病的临床过程会导致病人的预后不佳。尤其这种病理性的肌肉损失影响了骨骼肌。到目前为止，其发生的分子信号通路尚未清楚。导致这种退化过程的其中一个原因是人体内调节血压和盐/水的供给系统（即所谓的肾素-血管紧张素-醛固酮系统(RAAS)）。在疾病过程的环境中RAAS可被强烈激活，且与心源性恶病质相关，导致效应器肽血管紧


发达国家心肌功能不全的患者通常会伴有肌肉损耗和肌肉力量的下降。事实上直到现在，消极影响疾病的临床过程会导致病人的预后不佳。尤其这种病理性的肌肉损失影响了骨骼肌。到目前为止，其发生的分子信号通路尚未清楚。导致这种退化过程的其中一个原因是人体内调节血压和盐/水的供给系统（即所谓的肾素-血管紧张素-醛固酮系统(RAAS)）。在疾病过程的环境中RAAS可被强烈激活，且与心源性恶病质相关，导致效应器肽血管紧张素II的形成升高。血管紧张素II可直接影响肌肉并加强蛋白质的降解，导致肌肉损失和肌肉强度的下降。

到目前为止，治疗心力衰竭患者的药物可抑制肾素-血管紧张素-醛固酮系统。虽然这种治疗方法可在一段时间内减缓肌肉损失，但是这种药物的疗效仅能维持几年。为了寻找新的治疗方法，科学家与Dr. Jens Fielitz合作检测了表示肌肉中蛋白质降解的精准的信号通路。尤其是，血管紧张素II增加了肌肉中某特定蛋白质（肌肉无名指1(MuRF1)）的水平， 该蛋白在肌肉损失中起着关键作用。

“我们已经能够识别并表征调节这一过程的一个新的转录因子的功能。我们的实验也揭示了激活或抑制MuRF1蛋白质的水平的具体机制，也就是说可减少或增加肌肉损失的程度，”Dr. Jens Fielitz说道，“我们的研究发现可为重要且悬而未决问题提供深刻的理解，在这个问题中他们描绘了一个对心源性恶病质的出现非常重要新的信号通路。”通过抑制这种信号通路或可抑制因血管紧张素II形成所造成的肌肉损失，并因此提供一种非常有前景的治疗方案。

原始出处：

Du Bois P1, Pablo Tortola C1, Lodka D1, Kny M1, Schmidt F1, Song K2, Schmidt S1, Bassel-Duby R3, Olson EN3, Fielitz J4.Angiotensin II Induces Skeletal Muscle Atrophy by Activating TFEB-Mediated MuRF1 Expression.Circ Res. 2015 Jul 2. pii: CIRCRESAHA.114.305393. [Epub ahead of print]

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    2016-04-04 旅苦化文_208

    #科学家发现#

    0

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    2015-08-14 yuanming7

    #心衰患者#

    0

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    2015-08-14 wgx310

    #信号通路#

    0

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    2015-08-13 Messichen1992

    跟进

    0

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    2015-08-13 Messichen1992

    心脏也不过是块肌肉

    0

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    2015-08-13 Messichen1992

    有意思的研究

    0

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    2015-08-13 Messichen1992

    期待早日用于临床

    0