Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.2
4.8
Journals
Biomolecules
Special Issues
Calcium Signaling in Cell Function and Dysfunction
share announcement

Calcium Signaling in Cell Function and Dysfunction

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 1241

Special Issue Editors

Dr. Giorgia Pallafacchina

E-Mail Website
Guest Editor
1. Neuroscience Institute, CNR (Italian National Research Council), Padua, Italy
2. Department of Biomedical Sciences, University of Padua, Padua, Italy
Interests: cell signaling; mitochondria; Ca2+ signaling; skeletal muscle; human pathology
Special Issues, Collections and Topics in MDPI journals
Dr. Sofia Zanin

E-Mail Website
Guest Editor
Laboratory for Genetics of Mitochondrial Disorders, UMR 1163, Institut Imagine, Université de Paris, Paris, France
Interests: mitochondrial diseases; gene therapy; mitochondrial metabolism; cell stress signalling; muscle

Special Issue Information

Dear Colleagues,

The role of Ca2+ signaling in the context of cell function and cell survival is undoubtedly crucial and universally recognized. Indeed, variations in the intracellular Ca2+ level have been associated with a plethora of different stimuli and cellular responses, from fertilization to neuronal transmission to muscle contraction and endocrine secretion, just to name the most renowned. As a consequence, the dynamics of Ca2+ signaling need to be finely orchestrated and tightly regulated within the cell; any eventual alteration of Ca2+ homeostasis is likely to lead to the impairment of cell functions, impacting on cell survival and eventually conducting to cell and organ dysfunction. It is no surprise that the presence of a defective Ca2+ handling is a common hallmark of many human pathologies, including neurodegeneration, cardiac failure, diabetes, muscle dystrophies and cancer. In this light, the aim of this Special Issue is to provide new evidence and revise the published literature about the role of Ca2+ signaling, and the associated regulatory machinery, in the context of cell and tissue function both in physiological conditions as well as in stress, damage and disease conditions.

Looking forward to receiving your contribution.

Sincerely,

Dr. Giorgia Pallafacchina
Dr. Sofia Zanin
Guest Editors

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 submissions that pass pre-check are 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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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.

Keywords

  • calcium signaling
  • calcium regulation
  • cell function
  • human pathology

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

13 pages, 1034 KiB  
Article
OGG1 Preserves Endothelial-Dependent Vasodilation and Regulates the Frequency and Spatial Area of Endothelial Calcium Signals
by Takreem Aziz, Larysa Yuzefovych, Lyudmila Rachek, Mark S. Taylor and Christopher M. Francis
Biomolecules 2025, 15(6), 790; https://doi.org/10.3390/biom15060790 - 29 May 2025
Viewed by 329
Abstract
Endothelial calcium dysregulation underlies impairments in endothelial-dependent vasodilation (EDV), contributing to vascular disease progression. Repletion of 8-oxoguanine DNA glycosylase (OGG1), an enzyme involved in base excision repair, has been shown to forestall vascular disease progression. However, the role of OGG1 in regulating endothelial [...] Read more.
Endothelial calcium dysregulation underlies impairments in endothelial-dependent vasodilation (EDV), contributing to vascular disease progression. Repletion of 8-oxoguanine DNA glycosylase (OGG1), an enzyme involved in base excision repair, has been shown to forestall vascular disease progression. However, the role of OGG1 in regulating endothelial calcium dynamics and in preserving EDV is unknown. Here, calcium imaging via high-speed confocal microscopy and automated analytics was used to quantify the spatial and temporal parameters of endothelial calcium signals in the excised carotid arteries of male and female C57BL6J/FVBNJ mice aged 4–7 months with normal endogenous levels of OGG1, in mice lacking OGG1, and in mice with repleted human OGG1 targeted to the mitochondria. Mice lacking OGG1 exhibited an anomalous calcium phenotype characterized by a substantial increase in the basal tissue-wide frequency and spatial area of the endothelial calcium signals. Mitochondrial repletion of hOGG1 restored the calcium phenotype under unstimulated and acetylcholine-stimulated conditions. EDV was assessed using pressure myography. Mice lacking OGG1 exhibited significant impairments in EDV in response to acetylcholine, and the mitochondrial repletion of OGG1 rescued EDV. These findings highlight a novel role for OGG1 in endothelial signaling and suggest its importance in vascular homeostasis. Full article
(This article belongs to the Special Issue Calcium Signaling in Cell Function and Dysfunction)
►▼ Show Figures

Figure 1

Review

Jump to: Research

54 pages, 2627 KiB  
Review
Calcium Signaling Dynamics in Vascular Cells and Their Dysregulation in Vascular Disease
by Chang Dai and Raouf A. Khalil
Biomolecules 2025, 15(6), 892; https://doi.org/10.3390/biom15060892 - 18 Jun 2025
Viewed by 422
Abstract
Calcium (Ca2+) signaling is a fundamental regulatory mechanism controlling essential processes in the endothelium, vascular smooth muscle cells (VSMCs), and the extracellular matrix (ECM), including maintaining the endothelial barrier, modulation of vascular tone, and vascular remodeling. Cytosolic free Ca2+ concentration [...] Read more.
Calcium (Ca2+) signaling is a fundamental regulatory mechanism controlling essential processes in the endothelium, vascular smooth muscle cells (VSMCs), and the extracellular matrix (ECM), including maintaining the endothelial barrier, modulation of vascular tone, and vascular remodeling. Cytosolic free Ca2+ concentration is tightly regulated by a balance between Ca2+ mobilization mechanisms, including Ca2+ release from the intracellular stores in the sarcoplasmic/endoplasmic reticulum and Ca2+ entry via voltage-dependent, transient-receptor potential, and store-operated Ca2+ channels, and Ca2+ elimination pathways including Ca2+ extrusion by the plasma membrane Ca2+-ATPase and Na+/Ca2+ exchanger and Ca2+ re-uptake by the sarco(endo)plasmic reticulum Ca2+-ATPase and the mitochondria. Some cell membranes/organelles are multifunctional and have both Ca2+ mobilization and Ca2+ removal pathways. Also, the individual Ca2+ handling pathways could be integrated to function in a regenerative, capacitative, cooperative, bidirectional, or reciprocal feed-forward or feed-back manner. Disruption of these pathways causes dysregulation of the Ca2+ signaling dynamics and leads to pathological cardiovascular conditions such as hypertension, coronary artery disease, atherosclerosis, and vascular calcification. In the endothelium, dysregulated Ca2+ signaling impairs nitric oxide production, reduces vasodilatory capacity, and increases vascular permeability. In VSMCs, Ca2+-dependent phosphorylation of the myosin light chain and Ca2+ sensitization by protein kinase-C (PKC) and Rho-kinase (ROCK) increase vascular tone and could lead to increased blood pressure and hypertension. Ca2+ activation of matrix metalloproteinases causes collagen/elastin imbalance and promotes vascular remodeling. Ca2+-dependent immune cell activation, leukocyte infiltration, and cholesterol accumulation by macrophages promote foam cell formation and atherosclerotic plaque progression. Chronic increases in VSMCs Ca2+ promote phenotypic switching to mesenchymal cells and osteogenic transformation and thereby accelerate vascular calcification and plaque instability. Emerging therapeutic strategies targeting these Ca2+-dependent mechanisms, including Ca2+ channel blockers and PKC and ROCK inhibitors, hold promise for restoring Ca2+ homeostasis and mitigating vascular disease progression. Full article
(This article belongs to the Special Issue Calcium Signaling in Cell Function and Dysfunction)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop