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Cells
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Sex Hormone Receptor Signals in Health
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Sex Hormone Receptor Signals in Health

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Reproductive Cells and Development".

Deadline for manuscript submissions: closed (15 July 2023) | Viewed by 4837

Special Issue Editor

Prof. Dr. Raghvendra Dubey

E-Mail Website
Guest Editor
Department for Reproductive Endocrinology, University Zurich, CH8952 Schlieren, Switzerland
Interests: sex hormones and cardiovascular pathophysiology: mechanism(s) of action and therapeutic insights
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Sex hormones, which constitute estrogen(s), progesterone, and androgen, play an important role in the biology and pathophysiology of multiple organs. Apart from the reproductive system, sex hormones can actively influence health by regulating cardiovascular, renal, immune, hepatic, brain/neuronal, gastrointestinal, dermal, and stem cell function. Importantly, sex hormones have been associated with both good (cardiovascular and renal protection) and bad effects (reproductive cancers). Cellular and biological actions of sex steroids are largely mediated via nuclear receptors. Estrogens mediate their biological effects via nuclear estrogen receptors (ER) α, ERβ or the membrane/endoplasmic receptor GPER, whereas progesterone and androgen mediate their actions via the progesterone receptor (PR) and androgen receptor (AR), respectively. The actions of sex steroids are dependent on the tissue distribution and expression of the various receptors or their isoforms. For example, ERα protects against cardiovascular disease, whereas ERβ induces anticarcinogenic actions. Moreover, ERα inhibits growth of vascular smooth muscle cells but induces growth of vascular endothelial cells. The differential actions of sex steroids are driven by co-activators and co-repressors which combine with the nuclear hormone–receptor complex. These steroid–receptor interactions play a key role in defining the beneficial and deleterious effects of sex hormones and contribute to the overall effects on health. In-depth understanding of the mechanism(s) of sex hormone signaling has led to a better understanding of hormone-associated diseases and the development of receptor-specific therapeutic agents. The aim of this Special Issue is to highlight the role of sex hormone receptors in the biology and pathophysiology of human health and to delineate cellular and molecular signaling mechanisms.

Prof. Dr. Raghvendra Dubey
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 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

  • Estrogen
  • Androgen
  • Cardiovascular
  • Estrogen receptors
  • Estrogen metabolism
  • 2-Methoxyestradiol
  • Vascular occlusion
  • Vascular remodeling
  • Atherosclerosis
  • Cardiovascular repair

Published Papers (2 papers)

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Research

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15 pages, 2912 KiB  
Article
PGRMC1 Ablation Protects from Energy-Starved Heart Failure by Promoting Fatty Acid/Pyruvate Oxidation
by Sang R. Lee, Moeka Mukae, Kang Joo Jeong, Se Hee Park, Hi Jo Shin, Sang Woon Kim, Young Suk Won, Hyo-Jung Kwun, In-Jeoung Baek and Eui-Ju Hong
Cells 2023, 12(5), 752; https://doi.org/10.3390/cells12050752 - 27 Feb 2023
Cited by 5 | Viewed by 2117
Abstract
Heart failure (HF) is an emerging epidemic with a high mortality rate. Apart from conventional treatment methods, such as surgery or use of vasodilation drugs, metabolic therapy has been suggested as a new therapeutic strategy. The heart relies on fatty acid oxidation and [...] Read more.
Heart failure (HF) is an emerging epidemic with a high mortality rate. Apart from conventional treatment methods, such as surgery or use of vasodilation drugs, metabolic therapy has been suggested as a new therapeutic strategy. The heart relies on fatty acid oxidation and glucose (pyruvate) oxidation for ATP-mediated contractility; the former meets most of the energy requirement, but the latter is more efficient. Inhibition of fatty acid oxidation leads to the induction of pyruvate oxidation and provides cardioprotection to failing energy-starved hearts. One of the non-canonical types of sex hormone receptors, progesterone receptor membrane component 1 (Pgrmc1), is a non-genomic progesterone receptor associated with reproduction and fertility. Recent studies revealed that Pgrmc1 regulates glucose and fatty acid synthesis. Notably, Pgrmc1 has also been associated with diabetic cardiomyopathy, as it reduces lipid-mediated toxicity and delays cardiac injury. However, the mechanism by which Pgrmc1 influences the energy-starved failing heart remains unknown. In this study, we found that loss of Pgrmc1 inhibited glycolysis and increased fatty acid/pyruvate oxidation, which is directly associated with ATP production, in starved hearts. Loss of Pgrmc1 during starvation activated the phosphorylation of AMP-activated protein kinase, which induced cardiac ATP production. Pgrmc1 loss increased the cellular respiration of cardiomyocytes under low-glucose conditions. In isoproterenol-induced cardiac injury, Pgrmc1 knockout resulted in less fibrosis and low heart failure marker expression. In summary, our results revealed that Pgrmc1 ablation in energy-deficit conditions increases fatty acid/pyruvate oxidation to protect against cardiac damage via energy starvation. Moreover, Pgrmc1 may be a regulator of cardiac metabolism that switches the dominance of glucose-fatty acid usage according to nutritional status and nutrient availability in the heart. Full article
(This article belongs to the Special Issue Sex Hormone Receptor Signals in Health)
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Review

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16 pages, 677 KiB  
Review
Estrogen Receptor Alpha Splice Variants, Post-Translational Modifications, and Their Physiological Functions
by Kenji Saito and Huxing Cui
Cells 2023, 12(6), 895; https://doi.org/10.3390/cells12060895 - 14 Mar 2023
Cited by 3 | Viewed by 2177
Abstract
The importance of estrogenic signaling for a broad spectrum of biological processes, including reproduction, cancer development, energy metabolism, memory and learning, and so on, has been well documented. Among reported estrogen receptors, estrogen receptor alpha (ERα) has been known to be a major [...] Read more.
The importance of estrogenic signaling for a broad spectrum of biological processes, including reproduction, cancer development, energy metabolism, memory and learning, and so on, has been well documented. Among reported estrogen receptors, estrogen receptor alpha (ERα) has been known to be a major mediator of cellular estrogenic signaling. Accumulating evidence has shown that the regulations of ERα gene transcription, splicing, and expression across the tissues are highly complex. The ERα promoter region is composed of multiple leader exons and 5′-untranslated region (5′-UTR) exons. Differential splicing results in multiple ERα proteins with different molecular weights and functional domains. Furthermore, various post-translational modifications (PTMs) further impact ERα cellular localization, ligand affinity, and therefore functionality. These splicing isoforms and PTMs are differentially expressed in a tissue-specific manner, mediate certain aspects of ERα signaling, and may work even antagonistically against the full-length ERα. The fundamental understanding of the ERα splicing isoforms in normal physiology is limited and association studies of the splicing isoforms and the PTMs are scarce. This review aims to summarize the functional diversity of these ERα variants and the PTMs in normal physiological processes, particularly as studied in transgenic mouse models. Full article
(This article belongs to the Special Issue Sex Hormone Receptor Signals in Health)
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