Skeletal and cardiac muscle calcium transport regulation in health and disease

In healthy muscle, the rapid release of calcium ions (Ca2+) with excitation-contraction (E-C) coupling, results in elevations in Ca2+ concentrations which can exceed 10-fold that of rest-ing values. The sizable transient changes in Ca2+ concentrations are necessary for the ac-tivation of signaling pathways, which rely on Ca2+ as a second messenger, including those involved with force generation, fiber type distribution and hypertrophy. However, prolonged elevations in intracellular Ca2+ can result in the unwanted activation of Ca2+ signaling path-ways that cause muscle damage, dysfunction, and disease. Muscle employs several cal-cium handling and calcium transport proteins that function to rapidly return Ca2+ concen-trations back to resting levels following contraction. This review will detail our current under-standing of calcium handling during the decay phase of intracellular calcium transients in healthy skeletal and cardiac muscle. We will also discuss how impairments in Ca2+ transport can occur and how mishandling of Ca2+ can lead to the pathogenesis and/or progression of skeletal muscle myopathies and cardiomyopathies.

Automated summary

This article discusses the release and transport of calcium ions in healthy muscle, and the impact of changes in calcium ion concentrations on signaling pathways. It also explores the relationship between calcium ion transport impairments and the pathogenesis of skeletal muscle myopathies and cardiomyopathies.