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Calcium Handling in Cell Physiology and Pathophysiology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1180

Special Issue Editor

Special Issue Information

Dear Colleagues,

Calcium ions (Ca2+) handling is the central coordinator of the functions of excitable cells. For neuronal, skeletal, cardiac or smooth muscle, and for pancreatic beta cells, the transient elevation of intracellular Ca2+ triggers molecular machines and produces key cellular responses such as contraction and secretion. Beyond this role in excitable cells, the acute elevation of intracellular Ca2+ concentration produces universal cellular physiologic responses affecting cellular shape, motility, gene expression, growth or apoptosis. Therefore, keeping the plasma membrane Ca2+ gradient between a high Ca2+ content (1.1–1.4 mM) in the extracellular fluid and the cytosol (0.15 μM), as well as maintaining the endoplasmic reticulum Ca2+ gradient (100.0 μΜ) and the mitochondria inner membrane Ca2+ buffering capacity (50.0 μM), is of critical importance in cell physiology and responsiveness. Upon excitation, these Ca2+ stores release Ca2+ to the cytosol, and getting the time to decay of cytosolic Ca2+ down by four orders of magnitude is equally important to judge between life and death conditions for the cell. These delicate, regulated processes are mediated through ion channels, accessory regulatory and Ca2+ buffering proteins of which mutations, functional deregulations or expression changes are frequently involved in pathophysiological situations that could be evolved in human diseases. As druggable agents, these proteins represent pharmacological targets for the treatment of neuronal, muscular, cardiological, endocrinal or homeostasis diseases. This Special Issue of IJMS (“Calcium Handling in Cell Physiology and Pathophysiology”) will present novel research and reviews in the field of Ca2+ handling proteins’ molecular interplay and regulation in cell physiology and pathophysiology.

Dr. Demetrios A. Arvanitis
Guest Editor

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Keywords

  • Ca2+
  • endoplasmic reticulum
  • mitochondria
  • neuron
  • skeletal muscle
  • cardiac muscle
  • smooth muscle
  • pancreatic beta cells
  • contractility
  • secretion

Published Papers (1 paper)

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Review

32 pages, 2206 KiB  
Review
Cracking the Endothelial Calcium (Ca2+) Code: A Matter of Timing and Spacing
by Francesco Moccia, Valentina Brunetti, Teresa Soda, Roberto Berra-Romani and Giorgia Scarpellino
Int. J. Mol. Sci. 2023, 24(23), 16765; https://doi.org/10.3390/ijms242316765 - 26 Nov 2023
Viewed by 952
Abstract
A monolayer of endothelial cells lines the innermost surface of all blood vessels, thereby coming into close contact with every region of the body and perceiving signals deriving from both the bloodstream and parenchymal tissues. An increase in intracellular Ca2+ concentration ([Ca [...] Read more.
A monolayer of endothelial cells lines the innermost surface of all blood vessels, thereby coming into close contact with every region of the body and perceiving signals deriving from both the bloodstream and parenchymal tissues. An increase in intracellular Ca2+ concentration ([Ca2+]i) is the main mechanism whereby vascular endothelial cells integrate the information conveyed by local and circulating cues. Herein, we describe the dynamics and spatial distribution of endothelial Ca2+ signals to understand how an array of spatially restricted (at both the subcellular and cellular levels) Ca2+ signals is exploited by the vascular intima to fulfill this complex task. We then illustrate how local endothelial Ca2+ signals affect the most appropriate vascular function and are integrated to transmit this information to more distant sites to maintain cardiovascular homeostasis. Vasorelaxation and sprouting angiogenesis were selected as an example of functions that are finely tuned by the variable spatio-temporal profile endothelial Ca2+ signals. We further highlighted how distinct Ca2+ signatures regulate the different phases of vasculogenesis, i.e., proliferation and migration, in circulating endothelial precursors. Full article
(This article belongs to the Special Issue Calcium Handling in Cell Physiology and Pathophysiology)
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