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Special Issue "Vitamin D and Its Analogues 2019: New Insights on Biological Effects and Therapeutic Uses"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 31 August 2019

Special Issue Editors

Lead Guest Editor
Prof. Dr. George P. Studzinski

Department of Pathology, Rutgers-New Jersey Medical School, Newark, NJ 17101, USA
Website | E-Mail
Interests: vitamin D; vitamin D analogs; cell differentiation; apoptosis; cytotoxic autophagy; nuclear receptors; intracellular signaling pathways; AML
Guest Editor
Prof. Dr. Michael Danilenko

Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer Sheva 84105, Israel
Website | E-Mail
Interests: acute myeloid leukemia; cell differentiation; vitamin D; vitamin D analogs; plant-derived bioactive compounds; redox signaling and regulation; calcium signaling; cell cycle regulation, apoptosis
Guest Editor
Prof. Dr. Ewa Marcinkowska

Department of Biotechnology, University of Wroclaw, Wroclaw, Poland
Website 1 | Website 2 | E-Mail
Interests: vitamin D; vitamin D analogs; retinoids; semi-selective activities; cell differentiation; nuclear receptors

Special Issue Information

Dear Colleagues,

The proven importance of vitamin D for human health has stimulated extensive efforts, not only to understand the variety of its biological actions, but also attempts by organic chemists to modify the vitamin D structure to produce analogs that can be more potent in its effects on various body systems other than the skeletal system. The earliest modification occurred in nature. Animals, including humans, synthesize the secosteroid known as vitamin D3 (cholecalciferol), while plants synthesize vitamin D2 (ergocalciferol) with an unsaturated side-chain. Both have similar biological functions in humans, and both are used to treat rickets, osteoporosis, and osteomalacia. In order to be active as regulators of gene transcription, they need to be metabolically activated in the human body. Vitamin D2 and its derivatives were found to be somewhat less potent, but also less toxic, compared to vitamin D3 compounds. Numerous analogues have been synthesized with the primary goal of overcoming the hypercalcemic toxicity of active natural vitamin D derivatives, which limits their clinical use. Several such analogues have demonstrated reduced calcemic effects in model systems and human studies. Nevertheless, more work is necessary to develop clinically effective analogues. The ability of vitamin D compounds to cooperate with conventional drugs and with agents that sensitize abnormal cells to these compounds may offer a complementary approach towards an improved vitamin D-based therapy of human diseases.

This Special Issue will cover a selection of recent research topics and current review articles in the field of vitamin D and its analogues for biological actions and therapy of human diseases.

Prof. Dr. Ewa Marcinkowska
Prof. Dr. George P. Studzinski
Prof. Dr. Michael Danilenko
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 papers will be 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. International Journal of Molecular Sciences 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 1800 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.


  • vitamin D
  • analogs of vitamin D
  • vitamin D receptor
  • vitamin D metabolism
  • calcium-phosphate homeostasis
  • differentiation
  • apoptosis
  • cell cycle
  • intracellular signaling
  • regulation of immune system

Published Papers (1 paper)

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Open AccessArticle
25-Hydroxyvitamin D Inhibits Hepatitis C Virus Production in Hepatocellular Carcinoma Cell Line by a Vitamin D Receptor-Independent Mechanism
Int. J. Mol. Sci. 2019, 20(9), 2367; https://doi.org/10.3390/ijms20092367
Received: 20 March 2019 / Revised: 7 May 2019 / Accepted: 10 May 2019 / Published: 13 May 2019
PDF Full-text (1473 KB) | HTML Full-text | XML Full-text | Supplementary Files
Previously, we have reported that the active vitamin D metabolite, calcitriol and vitamin D3 (cholecalciferol), both remarkably inhibit hepatitis C virus production. The mechanism by which vitamin D3 exerts its effect is puzzling due to the low levels of calcitriol produced [...] Read more.
Previously, we have reported that the active vitamin D metabolite, calcitriol and vitamin D3 (cholecalciferol), both remarkably inhibit hepatitis C virus production. The mechanism by which vitamin D3 exerts its effect is puzzling due to the low levels of calcitriol produced in vitamin D3-treated Huh7.5 cells. In this study, we aimed to explore the mechanism of vitamin D3 anti-hepatitis C virus effect. We show that vitamin D3 activity is not mediated by its metabolic conversion to calcitriol, but may be due to its primary metabolic product 25(OH)D3. This is inferred from the findings that 25(OH)D3 could inhibit hepatitis C virus production in our system, and that adequate concentrations needed to exert this effect are produced in Huh7.5 cells treated with vitamin D3. Using the CRISPR-Cas9 editing technology to knockout the vitamin D receptor, we found that the antiviral activity of vitamin D3 and 25(OH)D3 was not impaired in the vitamin D receptor knockout cells. This result indicates that 25(OH)D3 anti-hepatitis C virus effect is exerted by a vitamin D receptor-independent mode of action. The possibility that vitamin D3 and 25(OH)D3, being 3β-hydroxysteroids, affect hepatitis C virus production by direct inhibition of the Hedgehog pathway in a vitamin D receptor-independent manner was ruled out. Taken together, this study proposes a novel mode of action for the anti-hepatitis C virus activity of vitamin D3 that is mediated by 25(OH)D3 in a vitamin D receptor-independent mechanism. Full article

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Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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