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摘要
癌症恶病质是一种使人衰弱的副肿瘤综合征。它的特点是骨骼肌消耗和体重下降。它影响了50-80%的癌症患者,并且直接占因心肺衰竭癌症死亡的25%。肌肉无力,这种综合征的标志之一,已被假定为是由于肌肉分解,功能障碍和减少的修复能力以及当前限制的有效治疗策略导致的。由于宿主肿瘤的作用,如白细胞介素(IL)6和肿瘤坏死因子(TNF)-α导致了过度的炎症细胞因子的水平被假设以驱动这一病理过程,而使这些细胞因子在癌性恶病质中产生骨骼肌功能障碍的具体机制尚不明确。内质网应激(ER)和钙信号相关的中断在骨骼肌和功能的细胞因子介导的中断中十分重要。中断的内质网应激过程如未折叠蛋白反应(UPR),钙稳态以及改变肌肉蛋白质的合成已在临床和实验性恶病质等炎症驱动肌肉疾病如肌炎中报道,可能与这之间增加的IL-6和TNF-α以及骨骼肌细胞中的内质网应激有关系。在骨骼肌细胞中,由于增加的细胞因子的上调的内质网应力的概念是新的并潜在的与我们对癌症恶病质的理解十分相关,本文旨在探讨炎性细胞因子与肌肉分解和ER应激介导之间的潜在关系,在癌症恶病质的内容中,去探讨其分子信号通路的基础病理学。
关键词: 骨骼肌;癌性恶病质;内质网;蛋白质转换;钙;细胞因子。
Current Drug Targets
Title:Endoplasmic Reticulum Stress, Calcium Dysregulation and Altered Protein Translation: Intersection of Processes That Contribute to Cancer Cachexia Induced Skeletal Muscle Wasting
Volume: 17 Issue: 10
Author(s): Stephanie T. Isaac, Timothy C. Tan, Patsie Polly
Affiliation:
关键词: 骨骼肌;癌性恶病质;内质网;蛋白质转换;钙;细胞因子。
摘要: Cancer cachexia is a debilitating paraneoplastic wasting syndrome characterized by skeletal muscle depletion and unintentional weight loss. It affects up to 50-80% of patients with cancer and directly accounts for one-quarter of cancer-related deaths due to cardio-respiratory failure. Muscle weakness, one of the hallmarks of this syndrome, has been postulated to be due to a combination of muscle breakdown, dysfunction and decrease in the ability to repair, with effective treatment strategies presently limited. Excessive inflammatory cytokine levels due to the host-tumor interaction, such as Interleukin (IL)-6 and Tumor Necrosis Factor (TNF)-α, are hypothesised to drive this pathological process but the specific mechanisms by which these cytokines produce skeletal muscle dysfunction in cancer cachexia remain undefined. Endoplasmic Reticulum (ER) stress and the associated disruptions in calcium signaling have been implicated in cytokine-mediated disruptions in skeletal muscle and function. Disrupted ER stress-related processes such as the Unfolded Protein Response (UPR), calcium homeostasis and altered muscle protein synthesis have been reported in clinical and experimental cachexia and other inflammation-driven muscle diseases such as myositis, potentially suggesting a link between increased IL-6 and TNF-α and ER stress in skeletal muscle cells. As the concept of upregulated ER stress in skeletal muscle cells due to elevated cytokines is novel and potentially very relevant to our understanding of cancer cachexia, this review aims to examine the potential relationship between inflammatory cytokine mediated muscle breakdown and ER stress, in the context of cancer cachexia, and to discuss the molecular signaling pathways underpinning this pathology.
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Stephanie T. Isaac, Timothy C. Tan, Patsie Polly , Endoplasmic Reticulum Stress, Calcium Dysregulation and Altered Protein Translation: Intersection of Processes That Contribute to Cancer Cachexia Induced Skeletal Muscle Wasting, Current Drug Targets 2016; 17 (10) . https://dx.doi.org/10.2174/1389450116666150416115721
DOI https://dx.doi.org/10.2174/1389450116666150416115721 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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