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Cells
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Advances in Hormonal Regulation of Calcium Homeostasis
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Advances in Hormonal Regulation of Calcium Homeostasis

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

Deadline for manuscript submissions: closed (20 June 2024) | Viewed by 3465

Special Issue Editors

Dr. Federica Saponaro

E-Mail Website
Guest Editor
Department of Pathology, University of Pisa, 56124 Pisa, Italy
Interests: hypoparathyroidism; hyperparathyroidism; parathyroid tumors; thyroid hormone analogs and metabolites; vitamin D metabolism; serum vitamin D levels and heart failure; endocrinology
Special Issues, Collections and Topics in MDPI journals
Dr. Giulia Battafarano

E-Mail Website
Guest Editor
Bone Physiopathology Research Unit, Translational Pediatrics and Clinical Genetics Research Division, Bambino Gesù Children’s Hospital, IRCCS, 00165 Rome, Italy
Interests: bone cancer; bone metabolism; bone turnover; bone cell pathophysiology; bone diseases in children
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Calcium metabolism homeostasis is maintained by refined hormonal control, which implicates the effects of three main players, namely PTH, Vitamin D and FGF23. This Special Issue welcomes original articles and reviews that address the mechanisms involved in the crosstalk among these hormones in the physiological and physiopathological contexts. Moreover, the pathological alterations involved in calcium-metabolism-related diseases will be addressed, with special attention paid to the following conditions: hyperparathyroidism, hypoparathyroidism, hypovitaminosis D and skeletal and extraskeletal effects, and FGF23 disturbance. We welcome the submission of original articles, partocularly those offerinng translational results.

Dr. Federica Saponaro
Dr. Giulia Battafarano
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

  • calcium metabolism
  • vitamin D
  • parathyroid hormone
  • FGF23
  • pathology
  • translational medicine

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Published Papers (2 papers)

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Research

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14 pages, 1576 KiB  
Article
VDR and PDIA3 Are Essential for Activation of Calcium Signaling and Membrane Response to 1,25(OH)2D3 in Squamous Cell Carcinoma Cells
by Joanna I. Nowak, Anna M. Olszewska, Justyna M. Wierzbicka, Magdalena Gebert, Rafał Bartoszewski and Michał A. Żmijewski
Cells 2024, 13(1), 11; https://doi.org/10.3390/cells13010011 - 20 Dec 2023
Cited by 4 | Viewed by 2314
Abstract
The genomic activity of 1,25(OH)2D3 is mediated by vitamin D receptor (VDR), whilst non-genomic is associated with protein disulfide isomerase family A member 3 (PDIA3). Interestingly, our recent studies documented that PDIA3 is also involved, directly or indirectly, in the [...] Read more.
The genomic activity of 1,25(OH)2D3 is mediated by vitamin D receptor (VDR), whilst non-genomic is associated with protein disulfide isomerase family A member 3 (PDIA3). Interestingly, our recent studies documented that PDIA3 is also involved, directly or indirectly, in the modulation of genomic response to 1,25(OH)2D3. Moreover, PDIA3 was also shown to regulate cellular bioenergetics, possibly through the modulation of STAT signaling. Here, the role of VDR and PDIA3 proteins in membrane response to 1,25(OH)2D3 and calcium signaling was investigated in squamous cell carcinoma A431 cell line with or without the deletion of VDR and PDIA3 genes. Calcium influx was assayed by Fura-2AM or Fluo-4AM, while calcium-regulated element (NFAT) activation was measured using a dual luciferase assay. Further, the levels of proteins involved in membrane response to 1,25(OH)2D3 in A431 cell lines were analyzed via Western blot analysis. The deletion of either PDIA3 or VDR resulted in the decreased baseline levels of Ca2+ and its responsiveness to 1,25(OH)2D3; however, the effect was more pronounced in A431∆PDIA3. Furthermore, the knockout of either of these genes disrupted 1,25(OH)2D3-elicited membrane signaling. The data presented here indicated that the VDR is essential for the activation of calcium/calmodulin-dependent protein kinase II alpha (CAMK2A), while PDIA3 is required for 1,25(OH)2D3-induced calcium mobilization in A431 cells. Taken together, those results suggest that both VDR and PDIA3 are essential for non-genomic response to this powerful secosteroid. Full article
(This article belongs to the Special Issue Advances in Hormonal Regulation of Calcium Homeostasis)
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Review

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12 pages, 1252 KiB  
Review
Effects of Sodium–Glucose Cotransporter 2 Inhibitors on Calcium Homeostasis: Where We Stand Now
by Alessandro Cuttone, Anastasia Xourafa, Carmela Morace, Vittorio Cannavò, Francesca Maria Bueti, Giuseppe Mandraffino, Giovanni Squadrito, Giorgio Basile, Agostino Gaudio, Antonino Catalano, Giuseppina Tiziana Russo and Federica Bellone
Cells 2025, 14(10), 724; https://doi.org/10.3390/cells14100724 - 15 May 2025
Viewed by 152
Abstract
Diabetes mellitus has been knowingly associated with increased risk of fractures, so much so that skeletal fragility is considered a complication of diabetes. Determinants of bone fragility in this chronic condition are several, and the diabetes treatment choice could influence bone metabolism. Sodium-glucose [...] Read more.
Diabetes mellitus has been knowingly associated with increased risk of fractures, so much so that skeletal fragility is considered a complication of diabetes. Determinants of bone fragility in this chronic condition are several, and the diabetes treatment choice could influence bone metabolism. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have recently expanded the therapeutic armamentarium for type 2 diabetes mellitus (T2D); these antihyperglycemic drugs act by reducing renal glucose reabsorption in the proximal tubule and have a proven cardiorenal benefit. The role of SGLT2i towards phospho-calcium metabolism is still unclear, so we aimed to review the current evidence of the relationship between SGLT2i and calcium and phosphate homeostasis. The PubMed, Scopus, and Web of Knowledge databases were searched to identify original research articles, meta-analyses, and scientific reviews on effects on bone metabolism in T2D patients treated with SGLT2i. Emerging data indicate that SGLT2i may lead to a rise of bone turnover markers, promoting a lower skeletal bone density and an increased fracture risk on murine models, but in real-world studies, results are controversial. Therefore, more clinical trials are needed to further clarify this topic, and the effects of SGLT2i on calcium homeostasis remain to date poorly understood. Full article
(This article belongs to the Special Issue Advances in Hormonal Regulation of Calcium Homeostasis)
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