The Role of Calcium Signaling in Cardiac and Skeletal Muscle

Dear Colleagues,

We are pleased to invite you to contribute to a Special Issue focusing on “The Role of Calcium Signaling in Cardiac and Skeletal Muscle”. The increase in intracellular calcium (Ca²⁺_CYT) represents a key event that couples a physiological signal with force generation in muscle. There is a direct positive correlation between the force generated by contracting cardiac and skeletal muscle cells and Ca²⁺_CYT. The spatiotemporal properties of intracellular Ca²⁺ signals are controlled by a well-coordinated interplay between Ca²⁺-handling proteins that either elevate Ca²⁺_CYT (e.g., ion channels) or remove Ca²⁺ from the cytoplasm (e.g., pumps and transporters). The classical mechanism of muscle contraction in response to membrane depolarization, a process termed excitation–contraction coupling (ECC), is well understood under physiological conditions. During pathology, multiple pathways may contribute to changes in Ca²⁺_CYT, not only altering ECC and contractility, but also sensitizing other Ca²⁺-dependent pathways, leading to changes in gene transcription and, thus, affecting the structure, metabolism, and function of myocytes.

This Special Issue aims to highlight similarities and differences between both cell types and identify molecular mechanisms that alter Ca²⁺ signals underlying muscle weakness in diseased striated muscle. Changes in Ca²⁺ handling during pathology are often complex and specific to each muscle type. In this Special Issue, original research articles and reviews on cardiac and skeletal muscle cells are welcome. Research areas may include (but are not limited to) the following: excitation–contraction coupling, Ca²⁺-dependent transcription processes, Ca²⁺-sensing proteins, Ca²⁺-buffering proteins, TRP channels, SOCE and stretch-activated ion channels, and metabolic changes affecting Ca²⁺-handling mechanisms associated with oxidative stress or inflammation.

We look forward to receiving your contributions.

Kind regards,

Dr. Andreas Rinne
Dr. Florentina Pluteanu
Guest Editors

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