Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Hormone Signaling in Human Health and Diseases, 2nd Edition
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Hormone Signaling in Human Health and Diseases, 2nd Edition

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

Deadline for manuscript submissions: 20 March 2025 | Viewed by 5717

Special Issue Editor

Dr. Antonella Muscella

E-Mail Website
Guest Editor
Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali, Università del Salento, Provinciale Lecce-Monteroni, Centro Ecotekne, 73100 Lecce, Italy
Interests: signal transduction; hormones; apoptosis; autophagy; metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of the 2022 Special Issue “Hormone Signaling in Human Health and Diseases”.

Cell signaling is part of any communication process that regulates the basic activities of cells and coordinates all cellular actions. The ability of cells to perceive and respond correctly to their microenvironment underlies the development, repair of tissues, immunity and homeostasis of normal tissues. Errors in signaling interactions and cellular information processing are responsible for three large classes of non-infectious diseases: cancers, neurodegenerative disorders and metabolic syndromes (such as type 2 diabetes and atherosclerosis). These diseases are remarkably complex and difficult to treat, primarily because when the cellular signaling pathways responsible for homeostasis and the health of the body become dysregulated, they generate similarly stable disease states.

Health- and disease-related conditions are dynamic and positively and negatively regulated by different feedback loops acting between pathways. Hormones are common signaling agents. Understanding cell signaling, especially relating hormone signaling, and describing regulatory networks in healthy and diseased states will show which molecular components may be the prime targets for drug interventions to manage these diseases more effectively. This is accomplished by studying models that explain in mechanistic, molecular detail the way in which a detailed part of the hormone signaling pathway functions properly in health and abnormally in disease.

Dr. Antonella Muscella
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. 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

  • hormone
  • cell receptor
  • endocrine signaling
  • cancer
  • insulin
  • oestrogen
  • testosterone
  • angiotensin
  • gonadotropin
  • thyroid hormone

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

12 pages, 1753 KiB  
Article
The Absence of Thyroid-Stimulating Hormone Receptor Expression on Natural Killer T Cells: Implications for the Immune–Endocrine Interaction
by Emilia Adamska-Fita, Przemysław Wiktor Śliwka, Małgorzata Karbownik-Lewińska, Andrzej Lewiński and Magdalena Stasiak
Int. J. Mol. Sci. 2024, 25(21), 11434; https://doi.org/10.3390/ijms252111434 - 24 Oct 2024
Cited by 1 | Viewed by 858
Abstract
The expression of thyroid-stimulating hormone receptor (TSHR) has been documented on various immune cells, including B lymphocytes, T lymphocytes, Natural Killer (NK) cells, monocytes, and dendritic cells (DCs). Natural Killer T (NKT) cells serve as a crucial link between innate and adaptive immunity, [...] Read more.
The expression of thyroid-stimulating hormone receptor (TSHR) has been documented on various immune cells, including B lymphocytes, T lymphocytes, Natural Killer (NK) cells, monocytes, and dendritic cells (DCs). Natural Killer T (NKT) cells serve as a crucial link between innate and adaptive immunity, playing significant roles in immunological interactions and autoimmune diseases. The aim of the present study was to evaluate the presence of TSHR on NKT cells. Our research involved patients with thyroid disease, as well as healthy controls. Peripheral blood mononuclear cells (PBMCs) and, thereafter, NKT cells were isolated from 86 patients with benign nodular thyroid disease with and without autoimmune thyroid disease (AITD) (28 and 56 cases, respectively), and TSHR expression was analyzed using fluorescence-activated cell sorting (FACS). In order to confirm the results, the reverse-transcription polymerase chain reaction (RT-PCR) method was used in cells obtained from healthy individuals. Our findings obtained with application of the FACS method revealed that TSHR is not expressed on NKT cells in either AITD or non-AITD patients, though TSHR was detected in the total PBMC population (TSHR+ cells 2.77%). The absence of TSHR on NKT cells was further confirmed with RT-PCR in healthy individuals (p < 0.0001). These results questioned the previously suggested direct influence of NKT cells on AITD development. Full article
(This article belongs to the Special Issue Hormone Signaling in Human Health and Diseases, 2nd Edition)
►▼ Show Figures

Figure 1

16 pages, 4116 KiB  
Article
Activation of G Protein-Coupled Estrogen Receptor 1 (GPER) Attenuates Obesity-Induced Asthma by Switching M1 Macrophages to M2 Macrophages
by So-Eun Son and Dong-Soon Im
Int. J. Mol. Sci. 2024, 25(17), 9532; https://doi.org/10.3390/ijms25179532 - 2 Sep 2024
Viewed by 1045
Abstract
The prevalence of obesity-induced asthma increases in women after menopause. We hypothesized that the increase in obese asthma in middle-aged women results from estrogen loss. In particular, we focused on the acute action of estrogen through the G protein-coupled estrogen receptor 1 (GPER), [...] Read more.
The prevalence of obesity-induced asthma increases in women after menopause. We hypothesized that the increase in obese asthma in middle-aged women results from estrogen loss. In particular, we focused on the acute action of estrogen through the G protein-coupled estrogen receptor 1 (GPER), previously known as GPR30. We investigated whether GPER activation ameliorates obesity-induced asthma with a high-fat diet (HFD) using G-1, the GPER agonist, and G-36, the GPER antagonist. Administration of G-1 (0.5 mg/kg) suppressed HFD-induced airway hypersensitivity (AHR), and increased immune cell infiltration, whereas G-36 co-treatment blocked it. Histological analysis showed that G-1 treatment inhibited HFD-induced inflammation, fibrosis, and mucus hypersecretion in a GPER-dependent manner. G-1 inhibited the HFD-induced rise in the mRNA levels of pro-inflammatory cytokines in the gonadal white adipose tissue and lungs, whereas G-36 co-treatment reversed this effect. G-1 increased anti-inflammatory M2 macrophages and inhibited the HFD-induced rise in pro-inflammatory M1 macrophages in the lungs. In addition, G-1 treatment reversed the HFD-induced increase in leptin expression and decrease in adiponectin expression in the lungs and gonadal white adipose tissue. The results suggest that activation of GPER could be a therapeutic option for obesity-induced asthma. Full article
(This article belongs to the Special Issue Hormone Signaling in Human Health and Diseases, 2nd Edition)
►▼ Show Figures

Figure 1

17 pages, 888 KiB  
Article
Leptin Is Associated with Testosterone, Nutritional Markers, and Vascular Muscular Dysfunction in Chronic Kidney Disease
by Crina Claudia Rusu, Ina Kacso, Diana Moldovan, Alina Potra, Dacian Tirinescu, Maria Ticala, Remus Orasan, Cristian Budurea, Florin Anton, Ana Valea, Cosmina Ioana Bondor and Mara Carsote
Int. J. Mol. Sci. 2024, 25(14), 7646; https://doi.org/10.3390/ijms25147646 - 12 Jul 2024
Viewed by 1422
Abstract
Chronic kidney disease (CKD) causes specific hormonal disturbances, such as variations in leptin and testosterone levels and function. These disturbances can promote errors in signaling interaction and cellular information processing and can be implicated in the pathogenesis of atherosclerosis. This study investigates the [...] Read more.
Chronic kidney disease (CKD) causes specific hormonal disturbances, such as variations in leptin and testosterone levels and function. These disturbances can promote errors in signaling interaction and cellular information processing and can be implicated in the pathogenesis of atherosclerosis. This study investigates the factors that affect leptin in CKD patients and examines how leptin is related to markers of vascular disease. We conducted a cross-sectional study of 162 patients with CKD in pre-dialysis and dialysis stages. We recorded clinical and laboratory data, including leptin, testosterone, and subclinical atherosclerosis markers like brachial–ankle pulse wave velocity (ba PWV) in pre-dialysis CKD patients and flow-mediated vasodilation (FMD) and nitroglycerin-mediated vasodilation (NMD) in hemodialysis (HD) patients. Leptin was significantly correlated with testosterone in CKD pre-dialysis stages (p < 0.001) and also in HD (p = 0.026), with adipose tissue mass in pre-dialysis stages (p < 0.001), and also in HD (p < 0.001). In women HD patients, leptin correlated with NMD (p = 0.039; r = −0.379); in all HD patients, leptin correlated with C reactive protein (p = 0.007; r = 0.28) and parathormone (p = 0.039; r = −0.220). Our research emphasizes the connection between leptin, adipose tissue, and testosterone in all stages of CKD. Leptin was associated with NMD in HD women and correlated with inflammatory syndrome and parathyroid hormone in all HD patients. Full article
(This article belongs to the Special Issue Hormone Signaling in Human Health and Diseases, 2nd Edition)
►▼ Show Figures

Figure 1

16 pages, 3470 KiB  
Article
Androgens Modulate Bcl-2 Agonist of Cell Death (BAD) Expression and Function in Breast Cancer Cells
by Catia Morelli, Chiara Chiodo, Marta Claudia Nocito, Alessandro Cormace, Stefania Catalano, Diego Sisci, Rosa Sirianni, Ivan Casaburi, Sebastiano Andò and Marilena Lanzino
Int. J. Mol. Sci. 2023, 24(17), 13464; https://doi.org/10.3390/ijms241713464 - 30 Aug 2023
Cited by 2 | Viewed by 1395
Abstract
Androgen receptor (AR) expression in estrogen receptor-positive (ER+) breast cancer (BC) correlates with lower tumor grade and a better clinical outcome. Additionally, in normal mammary epithelium or ER+ BC preclinical models, androgens counteract basal/ER-dependent proliferation. Here, we report an additional mechanism, underlining the [...] Read more.
Androgen receptor (AR) expression in estrogen receptor-positive (ER+) breast cancer (BC) correlates with lower tumor grade and a better clinical outcome. Additionally, in normal mammary epithelium or ER+ BC preclinical models, androgens counteract basal/ER-dependent proliferation. Here, we report an additional mechanism, underlining the protective role exerted by AR. Specifically, the activation of intracellular AR upregulates the Bcl-2-family protein BAD, and TCGA database analyses show that in ER+ BC, BAD expression is associated with better disease-free survival. Ligand-activated AR influences its own and BAD cellular compartmentalization by enhancing levels in the nucleus, as well as in mitochondrial fractions. In both compartments, BAD exerts unconventional functions. In the nucleus, BAD and AR physically interact and, upon androgen stimulation, are recruited at the AP-1 and ARE sites within the cyclin D1 promoter region, contributing to explaining the anti-proliferative effect of androgens in BC cells. Androgens cause an enrichment in BAD and AR content in the mitochondria, correlated with a decrease in mitochondrial function. Thus, we have defined a novel mechanism by which androgens modulate BAD expression, its mitochondria localization, and nuclear content to force its ability to act as a cell cycle inhibitor, strengthening the protective role of androgen signaling in estrogen-responsive BCs. Full article
(This article belongs to the Special Issue Hormone Signaling in Human Health and Diseases, 2nd Edition)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop