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Special Issue "Steroid Metabolism in Human Health and Disease"

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

Deadline for manuscript submissions: 1 June 2020.

Special Issue Editor

Dr. Amit V. Pandey
Website
Guest Editor
Pediatric Endocrinology, Diabetology and Metabolism, University Children’s Hospital Bern And Department of Biomedical Research, University of Bern, Freiburgstrasse 15, 3010 Bern, Switzerland
Interests: steroid metabolism; steroidogenesis; pregnenolone; cytochrome P450; P450 oxidoreductase; CYP17A1; CYP19A1; androgens; estrogens

Special Issue Information

Dear Colleagues,

Steroid hormones are necessary for life, from salt balance by mineralocorticoids, sugar balance by glucocorticoids, to the growth, reproductive, and sexual functions of sex steroids.

Steroid hormones are synthesized from cholesterol, starting from conversion, to pregnenolone, which is then converted to many different metabolites in a series of metabolic reactions.

Defects in the steroid metabolism cause a wide range of disorders, including the most common endocrine disorder in women, polycystic ovary syndrome. Therefore, control of steroid hormones production and signalling is an attractive target for the treatment of many metabolic disorders, including hormonal dependent cancers (targeting CYP17A1 and the androgen receptor in prostate cancer, and aromatase in breast cancer).

This Special Issue will focus on the molecular biology and biochemistry of steroid hormones in health and disease, and potential topics of interest may include, but are not limited, to the following:

  1. Molecular, cellular, and structural biology of steroid hormone production, regulation, and signalling in humans.
  2. Genetics and pathology of metabolic disorders caused by the changes in steroid metabolism, including the study of human mutations causing disordered steroidogenesis.
  3. Novel genes and mechanisms regulating steroid biosynthesis.
  4. Targeting of steroid hormone production, regulation, and signalling in metabolic disorders, including hormone-dependent cancers, by drugs and protein therapeutics.

Through this Special Issue, we aim to provide the latest work on the topic of steroid metabolism in human health and disease by experts in the field to a broad range of readership.

Dr. Amit V. Pandey
Guest Editor

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. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Steroid biosynthesis
  • Steroidogenesis
  • Androgen
  • Estrogen
  • Hormone-dependent cancers
  • Metabolic disorders
  • Steroid metabolizing enzymes

Published Papers (2 papers)

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Research

Open AccessArticle
Differential ESR1 Promoter Methylation in the Peripheral Blood—Findings from the Women 40+ Healthy Aging Study
Int. J. Mol. Sci. 2020, 21(10), 3654; https://doi.org/10.3390/ijms21103654 - 21 May 2020
Abstract
Background Estrogen receptor α (ERα) contributes to maintaining biological processes preserving health during aging. DNA methylation changes of ERα gene (ESR1) were established as playing a direct role in the regulation of ERα levels. In this study, we hypothesized decreased DNA [...] Read more.
Background Estrogen receptor α (ERα) contributes to maintaining biological processes preserving health during aging. DNA methylation changes of ERα gene (ESR1) were established as playing a direct role in the regulation of ERα levels. In this study, we hypothesized decreased DNA methylation of ESR1 associated with postmenopause, lower estradiol (E2) levels, and increased age among healthy middle-aged and older women. Methods We assessed DNA methylation of ESR1 promoter region from dried blood spots (DBSs) and E2 from saliva samples in 130 healthy women aged 40–73 years. Results We found that postmenopause and lower E2 levels were associated with lower DNA methylation of a distal regulatory region, but not with DNA methylation of proximal promoters. Conclusion Our results indicate that decreased methylation of ESR1 cytosine-phosphate-guanine island (CpGI) shore may be associated with conditions of lower E2 in older healthy women. Full article
(This article belongs to the Special Issue Steroid Metabolism in Human Health and Disease)
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Open AccessArticle
MicroRNA 322 Aggravates Dexamethasone-Induced Muscle Atrophy by Targeting IGF1R and INSR
Int. J. Mol. Sci. 2020, 21(3), 1111; https://doi.org/10.3390/ijms21031111 - 07 Feb 2020
Abstract
Dexamethasone (Dex) has been widely used as a potent anti-inflammatory, antishock, and immunosuppressive agent. However, high dose or long-term use of Dex is accompanied by side effects including skeletal muscle atrophy, whose underlying mechanisms remain incompletely understood. A number of microRNAs (miRNAs) have [...] Read more.
Dexamethasone (Dex) has been widely used as a potent anti-inflammatory, antishock, and immunosuppressive agent. However, high dose or long-term use of Dex is accompanied by side effects including skeletal muscle atrophy, whose underlying mechanisms remain incompletely understood. A number of microRNAs (miRNAs) have been shown to play key roles in skeletal muscle atrophy. Previous studies showed significantly increased miR-322 expression in Dex-treated C2C12 myotubes. In our study, the glucocorticoid receptor (GR) was required for Dex to increase miR-322 expression in C2C12 myotubes. miR-322 mimic or miR-322 inhibitor was used for regulating the expression of miR-322. Insulin-like growth factor 1 receptor (IGF1R) and insulin receptor (INSR) were identified as target genes of miR-322 using luciferase reporter assays and played key roles in Dex-induced muscle atrophy. miR-322 overexpression promoted atrophy in Dex-treated C2C12 myotubes and the gastrocnemius muscles of mice. Conversely, miR-322 inhibition showed the opposite effects. These data suggested that miR-322 contributes to Dex-induced muscle atrophy via targeting of IGF1R and INSR. Furthermore, miR-322 might be a potential target to counter Dex-induced muscle atrophy. miR-322 inhibition might also represent a therapeutic approach for Dex-induced muscle atrophy. Full article
(This article belongs to the Special Issue Steroid Metabolism in Human Health and Disease)
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