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一条与癌症恶病质相关的转化生长因子-β信号通路。

A TGF-β pathway associated with cancer cachexia.

作者信息

Guttridge Denis C

机构信息

Department of Molecular Virology, Immunology and Medical Genetics, Arthur G. James Comprehensive Cancer Center, The Ohio State University College of Medicine, Columbus, Ohio, USA.

出版信息

Nat Med. 2015 Nov;21(11):1248-9. doi: 10.1038/nm.3988.

DOI:10.1038/nm.3988
PMID:26540384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4896299/
Abstract

Cancer cachexia leads to involuntary weight loss resulting from the atrophy of skeletal muscle and adipose tissues. Now, in metastatic mouse models of cancer, investigators reveal a cross talk pathway between bone and muscle that provides a new understanding of wasting in advanced cancers.

摘要

癌症恶病质会导致骨骼肌和脂肪组织萎缩,进而引起非自愿性体重减轻。如今,在癌症转移小鼠模型中,研究人员揭示了骨骼与肌肉之间的一种相互作用途径,这为深入了解晚期癌症中的消瘦现象提供了新的视角。

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本文引用的文献

1
Excess TGF-β mediates muscle weakness associated with bone metastases in mice.过量的转化生长因子-β介导小鼠骨转移相关的肌肉无力。
Nat Med. 2015 Nov;21(11):1262-1271. doi: 10.1038/nm.3961. Epub 2015 Oct 12.
2
Ryanodine receptor oxidation causes intracellular calcium leak and muscle weakness in aging.肌质网钙释放通道氧化导致衰老过程中的细胞内钙泄漏和肌肉无力。
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Hypernitrosylated ryanodine receptor calcium release channels are leaky in dystrophic muscle.高亚硝基化的兰尼碱受体钙释放通道在营养不良性肌肉中存在渗漏。
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