Abstract
Investigations on ion channels in muscle tissues have mainly focused on physiological muscle function and related disorders, but emerging evidence supports a critical role of ion channels and transporters in developmental processes, such as controlling the myogenic commitment of stem cells. In this review, we provide an overview of ion channels and transporters that influence skeletal muscle myoblast differentiation, cardiac differentiation from pluripotent stem cells, as well as vascular smooth muscle cell differentiation. We highlight examples of model organisms or patients with mutations in ion channels. Furthermore, a potential underlying molecular mechanism involving hyperpolarization of the resting membrane potential and a series of calcium signaling is discussed.
Highlights
IntroductionThe movement of living organisms and the functioning of various visceral organs rely on muscle contraction and relaxation
[123,124,125] and pharmacological blockade of NCX1 impacted on CaMKII signaling to downregulate the expression of key cardiac markers (Nkx2.5, Myh6, and Tnnt2), which led to impaired differentiation and failure of cardiac crescent formation
It is becoming increasingly clear that ion channels and transporters play conserved roles in developmental processes [151]
Summary
The movement of living organisms and the functioning of various visceral organs rely on muscle contraction and relaxation These processes are controlled by endogenous bioelectric signaling mediated by ion channels and transporters. Mutations that disrupt the voltage-gated chloride channel ClC-1 [5,6,7] and the voltage-gated sodium channel Nav 1.4 [8,9] result in myotonia congenita and paramyotonia congenita, respectively Ion channels and their pathogenic roles have been extensively studied in mature, excitable muscle cells [10,11,12,13]. An elevated intracellular Ca2+ concentration can result from Ca2+ influx through specific Ca2+ channels in the plasma membrane (voltage-gated, ligand-gated, or store-operated calcium channels) or membrane (voltage-gated, ligand-gated, or store-operated channels)reticulum, or by the by the release of Ca2+ from intracellular calcium stores such ascalcium the endoplasmic.
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