Role of defective Ca2+ signaling in skeletal muscle weakness: Pharmacological implications

被引：56

作者：

Agrawal, Akanksha ^{[1
]}

Suryakumar, Geetha ^{[1
]}

Rathor, Richa ^{[1
]}

机构：

[1] DRDO, Def Inst Physiol & Allied Sci, Lucknow Rd, Delhi 110054, India

来源：

JOURNAL OF CELL COMMUNICATION AND SIGNALING | 2018年 / 12卷 / 04期

关键词：

Calcium; Ryanodine receptor; RyR1; Muscle; Atrophy; CALCIUM-RELEASE CHANNEL; CARDIAC SARCOPLASMIC-RETICULUM; RYANODINE-RECEPTOR; ENDOPLASMIC-RETICULUM; S-NITROSYLATION; INOSITOL 1,4,5-TRISPHOSPHATE; CALMODULIN-BINDING; NITRIC-OXIDE; DIHYDROPYRIDINE RECEPTOR; MOLECULAR-CLONING;

D O I：

10.1007/s12079-018-0477-z

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The misbehaving attitude of Ca2+ 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+/Ca2+ 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.

引用

页码：645 / 659

页数：15

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