Special Issue "Mechanisms of Endocrine and Molecular Bone Regulation"
Deadline for manuscript submissions: 30 September 2021.
Interests: mechanisms of endocrine and bone regulation; rare endocrine and bone diseases; molecular signaling of hormones; regulation of calcium metabolism; Prader–Willi syndrome pathophysiology
2. Université Paris-Saclay, INSERM, Physiologie et Physiopathologie Endocriniennes, Le Kremlin-Bicêtre, France
Interests: pediatric endocrinology; bone; calcium and phosphate metabolism; growth
Bone regulation offers striking new opportunities for its better understanding. Integration between molecular and endocrine mechanisms reveals unexpected relationships. Discovery of new agents involved in bone development has opened wide perspectives for the physiology and treatment of bone diseases and osteoporosis. Systemic regulation of bone mass by hormones such as growth hormone and IGF1, sex steroids, but also neuroendocrine hormones like leptin, ghrelin, oxytocin or other putative regulators during development and beyond is prominent. New actors such as FGF23 have appeared. The control of bone mass under recruitment and differentiation of osteoblasts precursors, as well as the role of osteocyte under mechanic stimulation, remain a still largely unexplored area. Local paracrine regulators, namely linked to the sclerostin pathway, seem also prominent. The goal is to provide an integrative vision of the main systemic and local regulators of bone mass, with special regard to new therapeutic options.
Prof. Dr. Jean Pierre Salles
Prof. Agnes Linglart
Manuscript Submission Information
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- Bone mass
- Growth hormone
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: 11BHSD1 mediates the bone protective effects of glucocorticoids when administered in chronic inflammation
Authors: Chloe G Fenton, Simon W Jones, Andrew Filer Mark Cooper, Gareth G Lavery, Karim Raza, Ramon Langen, Rowan Hardy
Affiliation: University of Birmingham
Title: Sclerostin: from molecule to clinical biomarker
Authors: Ahmed Omran; Diana Atanasova; Filip Landgren; Per Magnusson
Affiliation: Department of Clinical Chemistry, and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden
Abstract: The regulation of bone remodeling is strongly dependent on Wnt signaling, where activation of the Wnt pathway leads to increased bone mass and inactivation leads to bone loss. Sclerostin, a 22-kDa glycoprotein encoded by the SOST gene, is mainly produced by osteocytes and is a critical regulator of bone formation through its inhibitory effect on Wnt signaling. Besides inhibiting bone formation and osteoblastogenesis, it has also been demonstrated that sclerostin stimulates osteoclastogenesis and bone resorption. The osteocyte network is a vast and highly complex communication network and orchestrate the function of osteoblasts and osteoclasts in response to both mechanical and hormonal cues. The expression of sclerostin is limited to mature osteocytes. Downregulation of the SOST gene and local Wnt signaling are required for the osteogenic response to mechanical loading. Sclerostin is also present in the circulation and evidence suggests that sclerostin might also exert an endocrine function. Different immunoassays for the assessment of serum sclerostin are commercially available; however, differences due to immunoassay variability have been reported. Second generation assays for sclerostin, designated as bioactive sclerostin, have recently been developed, which might overcome some of the reported methodological obstacles. Current knowledge of sclerostin, with a focus on osteogenesis and methodological aspects of modern immunoassays, is summarized in this review.
Title: AROMATASE MUTATION IN MEN: A CASE REPORT AND REVIEW OF THE LITERATURE
Authors: Nele A. Stumper; Hilke Wientgen; Leith Al-Hashimi; Hans-Werner Müller; Sarah Ohrndorf; Heide Siggelkow; Paula Hoff
Affiliation: Endokrinologikum Göttingen and Georg-August-Universität Göttingen, 37075 Göttingen, Germany
Abstract: (1) Background: The clinical relevance of aromatase to a functioning male metabolism has become evident since 1991, when cases of patients with estrogen deficiency caused by aromatase mutation were first described. Only few cases are known so far, which will now be presented in a case report and review of the literature. (2) Methods: All available publications since the first description in 1991 dealing with loss-of-function aromatase mutation in men were summarized and our care report added. (3) Results: The mutations that cause the aromatase protein to lose function lead to a rather heterogeneous clinical picture. It is, however, clear that estrogens play a central role in male patients, especially in bone metabolism. Most frequently, tall stature, unclosed epiphyseal joints, and osteoporosis are detected in affected individuals as a consequence of the change in hormonal status. (4) Conclusions: Despite aromatase deficiency being a rare disease, the study of the effects of estrogen on male bone development provides important insights for endocrine bone regulation. It has been demonstrated that androgens alone are not sufficient for adequate skeletal development in males. This work highlights the important role of estrogens in individual health and disease in men.
Title: Bone metabolic features in Multiple Endocrine Neoplasia Type 1
Authors: Maria Luisa Brandi; Francesca Marini
Affiliation: University of Florence, Medical School, Florence