Unknown

Dataset Information

0

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


ABSTRACT: 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.

SUBMITTER: Agrawal A 

PROVIDER: S-EPMC6235775 | biostudies-other | 2018 Dec

REPOSITORIES: biostudies-other

altmetric image

Publications

Role of defective Ca<sup>2+</sup> signaling in skeletal muscle weakness: Pharmacological implications.

Agrawal Akanksha A   Suryakumar Geetha G   Rathor Richa R  

Journal of cell communication and signaling 20180707 4


The misbehaving attitude of Ca<sup>2+</sup> 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<sup>2+</sup> exchange pump in detail an  ...[more]

Similar Datasets

| S-EPMC5548641 | biostudies-literature
| S-EPMC6172310 | biostudies-literature
| S-EPMC8492340 | biostudies-literature
| S-EPMC7749611 | biostudies-literature
| S-EPMC2765867 | biostudies-literature
| S-EPMC7479987 | biostudies-literature
| S-EPMC7450176 | biostudies-literature
| S-EPMC6538353 | biostudies-literature
| S-EPMC7387164 | biostudies-literature
| S-EPMC3744478 | biostudies-literature