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 643

Special Issue Editors


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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

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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

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Keywords

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

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Published Papers (1 paper)

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Research

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 208
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)
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