Vitamin D in Health and Disease—Honorary Special Issue Commemorating the Work of Dr. Luminita A. Stanciu

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 May 2025 | Viewed by 1791

Special Issue Editors


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Guest Editor
Department of Pharmacology, Toxicology and Clinic Pharmacology, Iuliu Hatieganu University of Medicine and Pharmacy, 400000 Cluj-Napoca, Romania
Interests: food allergy; pollen allergy; allergic rhinitis; vitamin D
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Pediatrics, Karamandaneio Children’s Hospital of Patra, Erithrou Stavrou 40, 26331 Patra, Greece
Interests: pediatric allergy; food allergy; asthma; allergic rhinitis; vitamin D
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The pleiotropic activity of vitamin D in maintaining human health presents a challenge for further research. One hundred years after McCollum et al. concluded that vitamin D is the key factor that cures rickets, many other roles of vitamin D are under investigation. Recently, an increasing number of basic and clinical studies have been conducted that try to point to the new functions of vitamin D that are unrelated to its actions on mineral metabolism. For example, vitamin D inhibits proliferation, induces the differentiation of cells of different linages, and it is essential for regeneration of the epithelial barrier and for the maturation of immune cells. Throughout her 25 years of scientific work, Dr. Luminita A Stanciu tried to discover new molecules or new roles of known molecules, like vitamin D, in innate and adaptive immunity.

This Special Issue focuses on the role of vitamin D in the regulation of various mammalian cells and processes in health and diseases, focusing on its modulator roles in the respiratory and cardiovascular system, immune system, metabolic disorders, infectious diseases, allergic conditions, cellular metabolism, and in many other conditions. There is still an ongoing debate about whether vitamin D should be considered a supplement, for prophylaxis, or if it should be considered as an adjunctive therapy for multiple disorders.

Dr. Corina I. Bocsan
Dr. Gavriela Maria Feketea
Guest Editors

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Keywords

  • vitamin D
  • immune cells
  • innate immunity
  • respiratory diseases
  • allergy
  • infections
  • metabolic disorders
  • cellular metabolism

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Published Papers (2 papers)

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Research

16 pages, 2379 KiB  
Article
Genetic Polymorphism of CYP2R1, CYP27A1, CYP27B1, and Vitamin D Metabolites Plasma Levels in Patients with Cardiovascular Disease: A Pilot Study
by Mohamed Abouzid, Łukasz Kruszyna, Dominika Kaczmarek, Leonid Kagan, Aniceta Ada Mikulska-Sauermann, Dorota Filipowicz, Matylda Resztak, Franciszek K. Główka and Marta Karaźniewicz-Łada
Biomolecules 2025, 15(5), 699; https://doi.org/10.3390/biom15050699 - 11 May 2025
Viewed by 220
Abstract
The active form of vitamin D, calcitriol (1,25(OH)2D3), is produced from 25(OH)D3 via enzymes encoded by CYP2R1, CYP27A1, and CYP27B1. Polymorphisms in these genes may alter vitamin D metabolism and increase cardiovascular disease risk. This [...] Read more.
The active form of vitamin D, calcitriol (1,25(OH)2D3), is produced from 25(OH)D3 via enzymes encoded by CYP2R1, CYP27A1, and CYP27B1. Polymorphisms in these genes may alter vitamin D metabolism and increase cardiovascular disease risk. This preliminary study investigated these polymorphisms in 27 patients with cardiovascular disease and 26 healthy volunteers using Polymerase Chain Reaction—Restriction Fragment Length Polymorphism (PCR-RFLP), while measuring 25(OH)D3 and 1,25(OH)2D3 concentrations by UPLC-MS/MS and ELISA, respectively. Among patients, those with the GT genotype of rs10877012 (CYP27B1) had higher 25(OH)D3 levels compared to other genotypes. Additionally, this polymorphism was associated with lower 1,25(OH)2D3 in TT homozygotes, suggesting reduced CYP27B1 activity. Furthermore, the TT genotype of rs6709815 (CYP27A1) was three times more prevalent in cardiac patients than in healthy controls, possibly indicating increased susceptibility to the disease. Although these findings suggest a genetic influence on vitamin D metabolism in cardiovascular disease, larger and more comprehensive studies are needed to confirm these associations. Full article
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16 pages, 1209 KiB  
Article
Vitamin D Decreases Susceptibility of CD4+ T Cells to HIV Infection by Reducing AKT Phosphorylation and Glucose Uptake: A Bioinformatic and In Vitro Approach
by John D. Loaiza, Jose Fernando Gómez, Daniel Muñoz-Escudero, Sandra M. Gonzalez, Timothy Kyle Eubank, Maria T. Rugeles, Ana Lucía Rodríguez-Perea and Wbeimar Aguilar-Jimenez
Biomolecules 2025, 15(3), 432; https://doi.org/10.3390/biom15030432 - 18 Mar 2025
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Abstract
Activated immune cells are highly susceptible to human immunodeficiency virus (HIV) infection. Vitamin D (VitD) induces antimicrobial responses and reduces cellular activation. We investigated VitD effects on HIV-1 replication, glucose uptake, and gene regulation using computational and in vitro approaches. CD4+ T [...] Read more.
Activated immune cells are highly susceptible to human immunodeficiency virus (HIV) infection. Vitamin D (VitD) induces antimicrobial responses and reduces cellular activation. We investigated VitD effects on HIV-1 replication, glucose uptake, and gene regulation using computational and in vitro approaches. CD4+ T cells from healthy male donors were treated with VitD and infected with HIV-1. After 72 h, p24 protein was measured to assess viral replication. VitD effects on anti- and pro-HIV genes were analyzed by a Boolean network model based on curated databases and the literature. CCR5 and CXCR4 coreceptor expression, AKT phosphorylation, and glucose uptake were evaluated by flow cytometry, and expression of some model-identified genes was quantified by qPCR. VitD reduced p24 by 53.2% (p = 0.0078). Boolean network modeling predicted that VitD upregulates antiviral, migration, and cell-differentiation related genes, while downregulating genes related to cellular activation, proliferation, glucose metabolism, and HIV replication, notably AKT1, CCNT1, SLC2A1, HIF1A, and PFKL. In vitro, VitD reduced AKT phosphorylation by 26.6% (p = 0.0156), transcription of CCNT1 by 22.7% (p = 0.0391), and glucose uptake by 22.8% (p = 0.0039) without affecting classic antiviral genes or coreceptor expression. These findings suggest an anti-HIV effect of VitD, mediated through AKT and glucose metabolism downmodulation, both involved in cell activation and HIV-1 replication. Full article
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