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Special Issue "Calcium Signaling in Human Health and Diseases 2.0"
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (15 August 2019).
Interests: Ca2+ signaling; angiogenesis; endothelial cells; endothelial progenitor cells; neurovascular coupling
Special Issues and Collections in MDPI journals
This Special Issue is a continuation of our previous Special Issue "Calcium Signaling in Human Health and Diseases" (https://www.mdpi.com/journal/ijms/special_issues/calcium_signaling).
Intracellular Ca2+ signals regulate a myriad of cellular functions, ranging from short-term responses, such as excitation–contraction coupling and stimulus–secretion coupling, to long-term processes, such as proliferation, gene expression, differentiation, motility, synaptic plasticity, programmed cell death (or apoptosis) and metabolism. It is, therefore, not surprising that any derangement of the multifaceted Ca2+ toolkit that shapes the elevation in intracellular Ca2+ concentration ([Ca2+]i) may lead to severe pathological disorders, including cancer, neurodegenerative diseases, heart failure, severe combined immunodeficiency (SCID), deafness, pancreatitis, hypertension, and so on. An increase in [Ca2+]i is shaped by the concerted interaction among the components of an extremely versatile network of channels, transporters, pumps and buffer that can be uniquely assembled by each cell type to generate intracellular Ca2+ signals with spatio-temporal properties precisely tailored to regulate specific functions. We are witnessing a fascinating period of ground-breaking discoveries in the Ca2+ signalling field, as testified by the identification of the first structural molecular components of the mitochondrial Ca2+ uniporter and permeability transition pore, by the discovery of many unexpected regulators of intracellular Ca2+ dynamics, such as p53, PML, and PTEN, and by the evidence that a growing number of pathologies is associated to mutations in Ca2+-permeable channels and/or Ca2+-regulated pathways. I am, therefore, pleased to invite all of you to participate to this Special Issue, "Calcium Signaling in Human Health and Diseases", by presenting your most recent research or ideas about the pathophysiological role of Ca2+. Experimental papers, up-to-date review articles, and commentaries are all welcome.
Dr. Francesco Moccia
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- Ca2+ signalling
- intracellular organelles
- plasma membrane
- ryanodine receptors
- ionotropic receptors
- metabotropic receptors
- TRP channels
- two-pore channels
- STIM and Orai