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本文引用的文献

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Clinical and Pathologic Findings of Korean Patients with RYR1-Related Congenital Myopathy.韩国RYR1相关先天性肌病患者的临床和病理表现
J Clin Neurol. 2018 Jan;14(1):58-65. doi: 10.3988/jcn.2018.14.1.58.
2
Oxidative protein modification alters proteostasis under acute hypobaric hypoxia in skeletal muscles: a comprehensive in vivo study.氧化蛋白修饰改变骨骼肌急性低压缺氧下的蛋白质稳态：一项全面的体内研究。
Cell Stress Chaperones. 2017 May;22(3):429-443. doi: 10.1007/s12192-017-0795-8. Epub 2017 Apr 19.
3
Misregulation of calcium-handling proteins promotes hyperactivation of calcineurin-NFAT signaling in skeletal muscle of DM1 mice.钙处理蛋白的调节异常促进了DM1小鼠骨骼肌中钙调神经磷酸酶-NFAT信号通路的过度激活。
Hum Mol Genet. 2017 Jun 15;26(12):2192-2206. doi: 10.1093/hmg/ddx109.
4
Dihydropyridine receptor (DHPR, CACNA1S) congenital myopathy.二氢吡啶受体（DHPR，CACNA1S）先天性肌病。
Acta Neuropathol. 2017 Apr;133(4):517-533. doi: 10.1007/s00401-016-1656-8. Epub 2016 Dec 23.
5
Spinal Cord Injury Leads to Hyperoxidation and Nitrosylation of Skeletal Muscle Ryanodine Receptor-1 Associated with Upregulation of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 4.脊髓损伤导致骨骼肌雷诺丁受体-1的过氧化和亚硝基化，与烟酰胺腺嘌呤二核苷酸磷酸氧化酶4的上调相关。
J Neurotrauma. 2017 Jun 15;34(12):2069-2074. doi: 10.1089/neu.2016.4763. Epub 2017 Feb 27.
6
How and why are calcium currents curtailed in the skeletal muscle voltage-gated calcium channels?骨骼肌电压门控钙通道中的钙电流是如何以及为何被缩减的？
J Physiol. 2017 Mar 1;595(5):1451-1463. doi: 10.1113/JP273423.
7
Core skeletal muscle ryanodine receptor calcium release complex.核心骨骼肌兰尼碱受体钙释放复合体
Clin Exp Pharmacol Physiol. 2017 Jan;44(1):3-12. doi: 10.1111/1440-1681.12676.
8
Role of the JP45-calsequestrin complex on calcium entry in slow twitch skeletal muscles.JP45-肌集钙蛋白复合物在慢肌骨骼肌钙内流中的作用。
J Biol Chem. 2016 Sep 23;291(39):20824. doi: 10.1074/jbc.A115.709071.
9
Ca handling abnormalities in early-onset muscle diseases: Novel concepts and perspectives.早期起病的肌肉疾病中钙处理异常：新概念和新视角。
Semin Cell Dev Biol. 2017 Apr;64:201-212. doi: 10.1016/j.semcdb.2016.07.017. Epub 2016 Jul 15.
10
Calcium Sparks in the Heart: Dynamics and Regulation.心脏中的钙火花：动力学与调节
Res Rep Biol. 2015;6:203-214. doi: 10.2147/RRB.S61495. Epub 2015 Oct 16.

钙信号缺陷在骨骼肌无力中的作用：药理学意义。

Role of defective Ca signaling in skeletal muscle weakness: Pharmacological implications.

作者信息

Agrawal Akanksha, Suryakumar Geetha, Rathor Richa

机构信息

DRDO, Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi, 110054, India.

出版信息

J Cell Commun Signal. 2018 Dec;12(4):645-659. doi: 10.1007/s12079-018-0477-z. Epub 2018 Jul 7.

DOI:10.1007/s12079-018-0477-z
PMID:29982883
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6235775/
Abstract

The misbehaving attitude of Ca signaling pathways could be the probable reason in many muscular disorders such as myopathies, systemic disorders like hypoxia, sepsis, cachexia, sarcopenia, heart failure, and dystrophy. The present review throws light upon the calcium flux regulating signaling channels like ryanodine receptor complex (RyR1), SERCA (Sarco-endoplasmic Reticulum Calcium ATPase), DHPR (Dihydropyridine Receptor) or Cav1.1 and Na+/Ca exchange pump in detail and how remodelling of these channels contribute towards disturbed calcium homeostasis. Understanding these pathways will further provide an insight for establishing new therapeutic approaches for the prevention and treatment of muscle atrophy under stress conditions, targeting calcium ion channels and associated regulatory proteins.

摘要

钙信号通路的异常行为可能是许多肌肉疾病的潜在原因，如肌病、全身性疾病如缺氧、败血症、恶病质、肌肉减少症、心力衰竭和营养不良。本综述详细阐述了调节钙通量的信号通道，如兰尼碱受体复合物（RyR1）、肌浆网钙ATP酶（SERCA）、二氢吡啶受体（DHPR）或Cav1.1以及钠/钙交换泵，以及这些通道的重塑如何导致钙稳态紊乱。了解这些通路将进一步为建立针对钙离子通道和相关调节蛋白的新治疗方法提供见解，以预防和治疗应激条件下的肌肉萎缩。