The Role of Calcium Signaling in Cardiac and Skeletal Muscle
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: 31 December 2025 | Viewed by 1200
Special Issue Editors
Interests: cardiac physiology; calcium signaling; GPCR signaling
Special Issue Information
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
Manuscript Submission Information
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Keywords
- striated muscle
- Ca2+ signaling
- excitation–contraction coupling
- remodeling
- inflammation
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