Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
4.9
Journals
IJMS
Special Issues
25th Anniversary of IJMS: Advances in Molecular Endocrinology and...
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

25th Anniversary of IJMS: Advances in Molecular Endocrinology and Metabolism

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: 31 December 2025 | Viewed by 3214

Special Issue Editor

Prof. Dr. José L. Quiles

grade E-Mail Website
Guest Editor
Department of Physiology, Institute of Nutrition and Food Technology “Jose Mataix”, Biomedical Research Center, University of Granada, Avda. Conocimiento s/n, 18100 Granada, Spain
Interests: cancer biology; antioxidants; oxidative stress; food chemistry; nutrition; reactive oxygen species
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

To celebrate the 25th anniversary of IJMS, this Special Issue highlights recent advances in molecular endocrinology and metabolism, including both classical and emerging topics. The collection features high-quality research and review articles covering hormonal regulation, metabolic diseases, neuroendocrinology, endocrine-related cancers, and aging, among other topics.

We also spotlight innovative technologies transforming the field, such as omics approaches, systems biology, and AI-driven analyses. We invite original and cross-disciplinary contributions that help unravel the complexity of endocrine systems and metabolic networks, and advance our understanding of human and comparative endocrinology.

Topics include, but are not limited to, the following:

  • Endocrine systems and endocrine-related diseases.
  • Molecular, cellular, genetic, epigenetic, and developmental approaches.
  • Animal models in endocrine and metabolic research.
  • Novel insights into physiology, pathophysiology, and therapeutic strategies.
  • Neuroendocrinology and neuroendocrine control of endocrine axes.
  • Classical glands: thyroid, adrenal, pituitary, parathyroid, testis, ovary, etc.
  • Non-classical endocrine systems: gut, bone, liver, etc.
  • Lipid and bone metabolism.
  • Hormones, paracrine factors, receptors, and binding proteins.
  • Nuclear and membrane hormone receptors and intracellular signaling pathways.
  • Steroid biosynthesis and metabolism of hormones and neurotransmitters.
  • Cellular interactions and regulatory factors in endocrine tissues.
  • Energy balance and expenditure.
  • Diabetes and insulin resistance.
  • Infertility and reproductive diseases.
  • Obesity and metabolic syndrome.
  • Osteoporosis and musculoskeletal endocrinology.
  • Aging and endocrine changes over the lifespan.
  • Endocrine-related tumors and cancers.
  • Endocrine-disrupting chemicals and environmental exposures.
  • Crossdisciplinary and integrative studies.
  • Comparative endocrinology.
  • Omics-based approaches (genomics, transcriptomics, proteomics, metabolomics, and lipidomics).
  • Systems biology and computational modeling of endocrine networks.
  • Artificial intelligence and machine learning in endocrine and metabolic research.
  • Microbiome–endocrine interactions.
  • Chronobiology and circadian regulation of hormonal systems.
  • Personalized and precision medicine in endocrinology.
  • Single-cell technologies and spatial transcriptomics applied to endocrine tissues.

Dr. José L. Quiles
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

  • molecular endocrinology
  • metabolic diseases
  • hormonal regulation
  • systems biology
  • precision medicine

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.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies 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

Jump to: Review

15 pages, 1833 KB  
Article
Relevance of STIM/Orai Calcium Entry System Hyperactivation in Human Prostate Contractility in Benign Prostate Hyperplasia
by José M. La Fuente, Mariam El Assar, Argentina Fernández, Leocadio Rodríguez-Mañas and Javier Angulo
Int. J. Mol. Sci. 2025, 26(18), 8985; https://doi.org/10.3390/ijms26188985 - 15 Sep 2025
Viewed by 100
Abstract
Benign prostate hyperplasia (BPH) is characterized by prostate enlargement and dynamic alterations contributing to development of lower tract urinary symptoms (LUTS). Prostate hypercontractility has been proposed to contribute to BPH-related LUTS. The aim was to evaluate the effects of inhibiting stromal interaction molecule [...] Read more.
Benign prostate hyperplasia (BPH) is characterized by prostate enlargement and dynamic alterations contributing to development of lower tract urinary symptoms (LUTS). Prostate hypercontractility has been proposed to contribute to BPH-related LUTS. The aim was to evaluate the effects of inhibiting stromal interaction molecule (STIM)/Orai calcium entry system on adrenergic and neurogenic contractions in prostate (HP) and bladder neck (HB) strips from BPH patients. Effects of STIM/Orai inhibition on adrenergic and neurogenic contractions of HP from organ donors (ODs) without BPH were also evaluated. HP and HB strips were obtained from 20 patients with BPH undergoing radical prostatectomy and from six OD at the time of organ collection for transplantation. Tissues were functionally evaluated for isometric tension recording. STIM-1, Orai1, and Orai3 protein expressions were determined in prostate tissues. STIM-1 was also localized by immunofluorescence in prostate sections. Norepinephrine-induced and neurogenic contractions were significantly reduced by STIM/Orai inhibition with YM-58483 (20 µM) in HP from BPH patients but not in tissues from ODs. STIM/Orai inhibition failed to significantly modify contraction of HB from BPH patients. Protein expression of STIM-1 was significantly elevated in HP from BPH patients. Functional contribution of STIM/Orai system to contractile tone is relevant in prostate when BPH is present, probably related to increased expression of STIM-1. Inhibition of STIM/Orai could have therapeutic implications for the management of BPH patients by alleviating prostatic hypercontraction. Full article
(This article belongs to the Special Issue 25th Anniversary of IJMS: Advances in Molecular Endocrinology and Metabolism)
►▼ Show Figures

Figure 1

20 pages, 3854 KB  
Article
Hepatic AhR Activation by TCDD Induces Obesity and Steatosis via Hepatic Plasminogen Activator Inhibitor-1 (PAI-1)
by Seung Jun Oh, Suyeol Im, Sora Kang, Aden Geonhee Lee, Byung Cheol Lee and Youngmi Kim Pak
Int. J. Mol. Sci. 2025, 26(17), 8452; https://doi.org/10.3390/ijms26178452 - 30 Aug 2025
Viewed by 541
Abstract
Exposure to persistent organic pollutants such as 2,3,7,8-tetrachlorodibenzodioxin (TCDD) increases metabolic disorder risk. In this study, we show that a single intraperitoneal injection of TCDD (10 μg/kg) in C57BL/6J mice induced body weight gain, lipid accumulation in the liver and adipose tissue, macrophage [...] Read more.
Exposure to persistent organic pollutants such as 2,3,7,8-tetrachlorodibenzodioxin (TCDD) increases metabolic disorder risk. In this study, we show that a single intraperitoneal injection of TCDD (10 μg/kg) in C57BL/6J mice induced body weight gain, lipid accumulation in the liver and adipose tissue, macrophage infiltration, and elevated hepatic and serum triglyceride levels after 12 weeks. Despite serum aryl hydrocarbon receptor (AhR) ligand levels normalizing by 12 weeks, the persistent effects suggest TCDD sequestration in fat tissue. TCDD inhibited the expression of mitochondrial proteins (COX1, TOM20, TFAM, H2AX) and reduced mitochondrial oxygen consumption. Liver-specific AhR knockout ameliorated TCDD-induced mitochondrial dysfunction, lipid accumulation, and macrophage infiltration. Mechanistically, TCDD-induced hepatic plasminogen activator inhibitor-1 (PAI-1) promoted adipocyte hypertrophy. In the liver, PAI-1 disrupted the interaction between tissue-type plasminogen activator (tPA) and apolipoprotein B (ApoB), thereby enhancing very-low-density lipoprotein (VLDL) assembly. These findings reveal that hepatocyte-derived circulating PAI-1, upregulated via hepatic AhR activation, contributes to adipocyte hypertrophy and hepatosteatosis through the intracellular modulation of the tPA–PAI-1 axis. Thus, hepatic AhR activation drives mitochondrial dysfunction and obesity, even after a single TCDD exposure. Full article
(This article belongs to the Special Issue 25th Anniversary of IJMS: Advances in Molecular Endocrinology and Metabolism)
►▼ Show Figures

Figure 1

Review

Jump to: Research

19 pages, 344 KB  
Review
Cushing’s Disease in the Animal Kingdom: Translational Insights for Human Medicine
by Elena Massardi, Germano Gaudenzi, Silvia Carra, Monica Oldani, Ilona Rybinska, Luca Persani and Giovanni Vitale
Int. J. Mol. Sci. 2025, 26(17), 8626; https://doi.org/10.3390/ijms26178626 - 4 Sep 2025
Viewed by 690
Abstract
Cushing’s disease (CD) is a rare neuroendocrine disorder caused by ACTH-secreting pituitary adenomas, presenting significant diagnostic and therapeutic challenges. Given the evolutionary conservation of the hypothalamic–pituitary–adrenal axis, this review explores the translational value of spontaneous CD forms in dogs, horses, cats, small mammals, [...] Read more.
Cushing’s disease (CD) is a rare neuroendocrine disorder caused by ACTH-secreting pituitary adenomas, presenting significant diagnostic and therapeutic challenges. Given the evolutionary conservation of the hypothalamic–pituitary–adrenal axis, this review explores the translational value of spontaneous CD forms in dogs, horses, cats, small mammals, and rats, as well as of experimental models in mice, rats, and zebrafish. Dogs are the most studied, showing strong molecular and clinical similarities with human CD, making them valuable for preclinical drug and diagnostic research. While equine and feline CD are less characterized, they may provide insights into dopaminergic therapies and glucocorticoid resistance. Nevertheless, practical and ethical challenges limit the experimental use of companion animals. In preclinical research, mouse models are widely used to study hypercortisolism and test therapeutic agents via transgenic and xenograft strategies. Conversely, few studies are available on a zebrafish transgenic model for CD, displaying pituitary corticotroph expansion and partial resistance to glucocorticoid-negative feedback at the larval stage, while adults exhibit hypercortisolism resembling the human phenotype. Future transplantable systems in zebrafish may overcome several limitations observed in mice, supporting CD research. Collectively, these animal models, each offering unique advantages and limitations, provide a diverse toolkit for advancing CD research and improving human clinical outcomes. Full article
(This article belongs to the Special Issue 25th Anniversary of IJMS: Advances in Molecular Endocrinology and Metabolism)
31 pages, 1732 KB  
Review
GLUT4 Trafficking and Storage Vesicles: Molecular Architecture, Regulatory Networks, and Their Disruption in Insulin Resistance
by Hana Drobiova, Ghadeer Alhamar, Rasheed Ahmad, Fahd Al-Mulla and Ashraf Al Madhoun
Int. J. Mol. Sci. 2025, 26(15), 7568; https://doi.org/10.3390/ijms26157568 - 5 Aug 2025
Viewed by 1513
Abstract
Insulin-regulated glucose uptake is a central mechanism in maintaining systemic glucose homeostasis, primarily occurring in skeletal muscle and adipose tissue. This process relies on the insulin-stimulated translocation of the glucose transporter, GLUT4, from specialized intracellular compartments, known as GLUT4 storage vesicles (GSVs), to [...] Read more.
Insulin-regulated glucose uptake is a central mechanism in maintaining systemic glucose homeostasis, primarily occurring in skeletal muscle and adipose tissue. This process relies on the insulin-stimulated translocation of the glucose transporter, GLUT4, from specialized intracellular compartments, known as GLUT4 storage vesicles (GSVs), to the plasma membrane. Disruption of this pathway is a hallmark of insulin resistance and a key contributor to the pathogenesis of type 2 diabetes. Recent advances have provided critical insights into both the insulin signalling cascades and the complex biogenesis, as well as the trafficking and fusion dynamics of GSVs. This review synthesizes the current understanding of the molecular mechanisms governing GSV mobilization and membrane fusion, highlighting key regulatory nodes that may become dysfunctional in metabolic disease. By elucidating these pathways, we propose new therapeutic avenues targeting GSV trafficking to improve insulin sensitivity and combat type 2 diabetes. Full article
(This article belongs to the Special Issue 25th Anniversary of IJMS: Advances in Molecular Endocrinology and Metabolism)
►▼ 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