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Cells
Special Issues
Calcium Signaling in Health and Diseases
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Calcium Signaling in Health and Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 25789

Special Issue Editors

Dr. Tim Vervliet

E-Mail Website
Guest Editor
KU Leuven Laboratory of Molecular Cellular Signaling, Department Cellular and Molecular Medicine, Leuven, Belgium
Interests: intracellular Ca2+ signaling; IP3R; ryanodine receptor (RyR); Bcl-2 protein family; apoptosis; autophagy; mitochondrial function; lysosomal function
Dr. Dhanendra Tomar

E-Mail Website
Guest Editor
Center for Translational Medicine, Lewis Katz School of Medicine of Temple University, Philadelphia, PA 19140, USA
Interests: mitochondria; calcium; post-translational modifications; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ca2+ signaling is involved in a myriad of cellular functions, including cell death, cell survival, autophagy, muscle contraction, and memory formation. Abnormalities in intracellular Ca2+ signaling have been shown to lead to defects in several organellar functions, resulting in cellular dysfunction and potential cell death. As such, it comes as no surprise that in numerous pathologies, dysregulated Ca2+ signaling plays a critical, early role in disease onset. Understanding how the cellular Ca2+ toolkit is organized and how it can be modulated is thus critical to further increase understanding of how pathologies arise and can be treated. Given the Ca2+ toolkit, its central role in many cellular functions provides a challenging yet interesting potential drug target pool to explore.

This Special Issue aims to highlight recent findings on how Ca2+ signaling regulates cellular functions, with the main focus being on how organellar function is affected in both physiological and pathophysiological conditions.

Dr. Tim Vervliet
Dr. Dhanendra Tomar
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. Cells is an international peer-reviewed open access semimonthly 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

  • Ca2+ signaling
  • organellar Ca2+
  • organellar contact sites
  • store-operated Ca2+ entry
  • neurodegenerative diseases
  • organellar (dys)function
  • mitochondria
  • lysosome
  • memory formation
  • aging
  • lysosomal storage disease

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Published Papers (4 papers)

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Research

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34 pages, 10606 KiB  
Article
Calreticulin Shortage Results in Disturbance of Calcium Storage, Mitochondrial Disease, and Kidney Injury
by Asima Tayyeb, Gry H. Dihazi, Björn Tampe, Michael Zeisberg, Desiree Tampe, Samy Hakroush, Charlotte Bührig, Jenny Frese, Nazli Serin, Marwa Eltoweissy, Gerhard A. Müller and Hassan Dihazi
Cells 2022, 11(8), 1329; https://doi.org/10.3390/cells11081329 - 13 Apr 2022
Cited by 3 | Viewed by 2864
Abstract
Renal Ca2+ reabsorption plays a central role in the fine-tuning of whole-body Ca2+ homeostasis. Here, we identified calreticulin (Calr) as a missing link in Ca2+ handling in the kidney and showed that a shortage of Calr results in mitochondrial disease [...] Read more.
Renal Ca2+ reabsorption plays a central role in the fine-tuning of whole-body Ca2+ homeostasis. Here, we identified calreticulin (Calr) as a missing link in Ca2+ handling in the kidney and showed that a shortage of Calr results in mitochondrial disease and kidney pathogenesis. We demonstrated that Calr+/− mice displayed a chronic physiological low level of Calr and that this was associated with progressive renal injury manifested in glomerulosclerosis and tubulointerstitial damage. We found that Calr+/− kidney cells suffer from a disturbance in functionally active calcium stores and decrease in Ca2+ storage capacity. Consequently, the kidney cells displayed an abnormal activation of Ca2+ signaling and NF-κB pathways, resulting in inflammation and wide progressive kidney injury. Interestingly, the disturbance in the Ca2+ homeostasis and signaling in Calr+/− kidney mice cells triggered severe mitochondrial disease and aberrant mitophagy, resulting in a high level of oxidative stress and energy shortage. These findings provide novel mechanistic insight into the role of Calr in kidney calcium handling, function, and pathogenesis. Full article
(This article belongs to the Special Issue Calcium Signaling in Health and Diseases)
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19 pages, 4370 KiB  
Article
Lauric Acid, a Dietary Saturated Medium-Chain Fatty Acid, Elicits Calcium-Dependent Eryptosis
by Mohammad A. Alfhili and Ghadeer S. Aljuraiban
Cells 2021, 10(12), 3388; https://doi.org/10.3390/cells10123388 - 1 Dec 2021
Cited by 16 | Viewed by 3692
Abstract
Cardiovascular diseases (CVD) are a leading cause of mortality worldwide, and dietary habits represent a major risk factor for dyslipidemia; a hallmark of CVD. Saturated fatty acids contribute to CVD by aggravating dyslipidemia, and, in particular, lauric acid (LA) raises circulating cholesterol levels. [...] Read more.
Cardiovascular diseases (CVD) are a leading cause of mortality worldwide, and dietary habits represent a major risk factor for dyslipidemia; a hallmark of CVD. Saturated fatty acids contribute to CVD by aggravating dyslipidemia, and, in particular, lauric acid (LA) raises circulating cholesterol levels. The role of red blood cells (RBCs) in CVD is increasingly being appreciated, and eryptosis has recently been identified as a novel mechanism in CVD. However, the effect of LA on RBC physiology has not been thoroughly investigated. RBCs were isolated from heparin-anticoagulated whole blood (WB) and exposed to 50–250 μM of LA for 24 h at 37 °C. Hemoglobin was photometrically examined as an indicator of hemolysis, whereas eryptosis was assessed by Annexin V-FITC for phosphatidylserine (PS) exposure, Fluo4/AM for Ca2+, light scatter for cellular morphology, H2DCFDA for oxidative stress, and BODIPY 581/591 C11 for lipid peroxidation. WB was also examined for RBC, leukocyte, and platelet viability and indices. LA caused dose-responsive hemolysis, and Ca2+-dependent PS exposure, elevated erythrocyte sedimentation rate (ESR), cytosolic Ca2+ overload, cell shrinkage and granularity, oxidative stress, accumulation of lipid peroxides, and stimulation of casein kinase 1α (CK1α). In WB, LA disrupted leukocyte distribution with elevated neutrophil-lymphocyte ratio (NLR) due to selective toxicity to lymphocytes. In conclusion, this report provides the first evidence of the pro-eryptotic potential of LA and associated mechanisms, which informs dietary interventions aimed at CVD prevention and management. Full article
(This article belongs to the Special Issue Calcium Signaling in Health and Diseases)
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Review

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23 pages, 14578 KiB  
Review
Dysregulated Ca2+ Homeostasis as a Central Theme in Neurodegeneration: Lessons from Alzheimer’s Disease and Wolfram Syndrome
by Manon Callens, Jens Loncke and Geert Bultynck
Cells 2022, 11(12), 1963; https://doi.org/10.3390/cells11121963 - 18 Jun 2022
Cited by 13 | Viewed by 4656
Abstract
Calcium ions (Ca2+) operate as important messengers in the cell, indispensable for signaling the underlying numerous cellular processes in all of the cell types in the human body. In neurons, Ca2+ signaling is crucial for regulating synaptic transmission and for [...] Read more.
Calcium ions (Ca2+) operate as important messengers in the cell, indispensable for signaling the underlying numerous cellular processes in all of the cell types in the human body. In neurons, Ca2+ signaling is crucial for regulating synaptic transmission and for the processes of learning and memory formation. Hence, the dysregulation of intracellular Ca2+ homeostasis results in a broad range of disorders, including cancer and neurodegeneration. A major source for intracellular Ca2+ is the endoplasmic reticulum (ER), which has close contacts with other organelles, including mitochondria. In this review, we focus on the emerging role of Ca2+ signaling at the ER–mitochondrial interface in two different neurodegenerative diseases, namely Alzheimer’s disease and Wolfram syndrome. Both of these diseases share some common hallmarks in the early stages, including alterations in the ER and mitochondrial Ca2+ handling, mitochondrial dysfunction and increased Reactive oxygen species (ROS) production. This indicates that similar mechanisms may underly these two disease pathologies and suggests that both research topics might benefit from complementary research. Full article
(This article belongs to the Special Issue Calcium Signaling in Health and Diseases)
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11 pages, 1007 KiB  
Review
Calcium Channels in the Heart: Disease States and Drugs
by Kajol Shah, Sarah Seeley, Castin Schulz, Jacqueline Fisher and Shubha Gururaja Rao
Cells 2022, 11(6), 943; https://doi.org/10.3390/cells11060943 - 10 Mar 2022
Cited by 42 | Viewed by 13251
Abstract
Calcium ions are the major signaling ions in the cells. They regulate muscle contraction, neurotransmitter secretion, cell growth and migration, and the activity of several proteins including enzymes and ion channels and transporters. They participate in various signal transduction pathways, thereby regulating major [...] Read more.
Calcium ions are the major signaling ions in the cells. They regulate muscle contraction, neurotransmitter secretion, cell growth and migration, and the activity of several proteins including enzymes and ion channels and transporters. They participate in various signal transduction pathways, thereby regulating major physiological functions. Calcium ion entry into the cells is regulated by specific calcium channels and transporters. There are mainly six types of calcium channels, of which only two are prominent in the heart. In cardiac tissues, the two types of calcium channels are the L type and the T type. L-type channels are found in all cardiac cells and T-type are expressed in Purkinje cells, pacemaker and atrial cells. Both these types of channels contribute to atrioventricular conduction as well as pacemaker activity. Given the crucial role of calcium channels in the cardiac conduction system, mutations and dysfunctions of these channels are known to cause several diseases and disorders. Drugs targeting calcium channels hence are used in a wide variety of cardiac disorders including but not limited to hypertension, angina, and arrhythmias. This review summarizes the type of cardiac calcium channels, their function, and disorders caused by their mutations and dysfunctions. Finally, this review also focuses on the types of calcium channel blockers and their use in a variety of cardiac disorders. Full article
(This article belongs to the Special Issue Calcium Signaling in Health and Diseases)
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