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Recent Research in Primary Osteoporosis: From a Bone Marrow Adiposity...
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Recent Research in Primary Osteoporosis: From a Bone Marrow Adiposity Perspective

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (10 May 2023) | Viewed by 3093

Special Issue Editor

Dr. Alexandrine During

E-Mail Website
Guest Editor
1. Marrow Adiposity and Bone Laboratory (MABLab) ULR4490, Université de Lille, 59000 Lille, France
2. CHU Lille, Université du Littoral Côte d'Opale, 62228 Calais, France
Interests: osteoporosis; anorexia nervosa; diabetis/obesity; osteo-articular diseases; bone marrow adiposity; adipogenesis/osteoblastogenesis; bone lipids; bone imaging

Special Issue Information

Dear Colleagues,

Primary osteoporosis (OP) type I (postmenopausal OP) and type II (age-associated OP) are characterized by bone mass loss and altered bone microarchitecture, ultimately resulting in an increased risk of fractures. In both OP types, bone mass is inversely correlated with medullary adiposity. Mounting evidence indicates that marrow adipocytes and their products of secretion may play a key role in skeletal pathophysiology, making them a potential target for new therapy development. This Special Issue will focus on the latest advances regarding our understanding on the role of marrow adiposity in the development of primary OP disease. Researchers are invited to submit original research and review articles covering significant developments in the field, ranging from basic to clinical studies. Interdisciplinary approaches are more than welcome, including molecular, cellular, bone tissue and individual aspects, as well as novel strategies targeting marrow adiposity that show promise in the prevention of primary OP.

Dr. Alexandrine During
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

  • ageing
  • postmenopausal status
  • bone loss and fracture risk
  • medullar adiposity
  • marrow adipocytes
  • adipokines
  • bone lipids
  • bone cells and tissue

Published Papers (2 papers)

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Research

14 pages, 310 KiB  
Article
Relationships between Circulating Sclerostin, Bone Marrow Adiposity, Other Adipose Deposits and Lean Mass in Post-Menopausal Women
by Marion Courtalin, Nicolas Bertheaume, Sammy Badr, Alexandrine During, Daniela Lombardo, Valérie Deken, Bernard Cortet, Aline Clabaut and Julien Paccou
Int. J. Mol. Sci. 2023, 24(6), 5922; https://doi.org/10.3390/ijms24065922 - 21 Mar 2023
Cited by 4 | Viewed by 1412
Abstract
Sclerostin is a Wnt signaling pathway inhibitor that negatively regulates bone formation. Bone-marrow-derived stromal cell (BMSC) differentiation is influenced by the Wnt pathway, leading to the hypothesis that higher levels of sclerostin might be associated with an increase in bone marrow adiposity (BMA). [...] Read more.
Sclerostin is a Wnt signaling pathway inhibitor that negatively regulates bone formation. Bone-marrow-derived stromal cell (BMSC) differentiation is influenced by the Wnt pathway, leading to the hypothesis that higher levels of sclerostin might be associated with an increase in bone marrow adiposity (BMA). The main purpose of this study was to determine whether a relationship exists between circulating sclerostin and BMA in post-menopausal women with and without fragility fractures. The relationships between circulating sclerostin and body composition parameters were then examined. The outcomes measures included vertebral and hip proton density fat fraction (PDFF) using the water fat imaging (WFI) MRI method; DXA scans; and laboratory measurements, including serum sclerostin. In 199 participants, no significant correlations were found between serum sclerostin and PDFF. In both groups, serum sclerostin was correlated positively with bone mineral density (R = 0.27 to 0.56) and negatively with renal function (R = −0.22 to −0.29). Serum sclerostin correlated negatively with visceral adiposity in both groups (R = −0.24 to −0.32). Serum sclerostin correlated negatively with total body fat (R = −0.47) and appendicular lean mass (R = −0.26) in the fracture group, but not in the controls. No evidence of a relationship between serum sclerostin and BMA was found. However, serum sclerostin was negatively correlated with body composition components, such as visceral adiposity, total body fat and appendicular lean mass. Full article
(This article belongs to the Special Issue Recent Research in Primary Osteoporosis: From a Bone Marrow Adiposity Perspective)
11 pages, 2091 KiB  
Article
Libanoridin Isolated from Corydalis heterocarpa Inhibits Adipogenic Differentiation of Bone Marrow-Derived Mesenchymal Stromal Cells
by Fatih Karadeniz, Jung Hwan Oh, Mi Soon Jang, Youngwan Seo and Chang-Suk Kong
Int. J. Mol. Sci. 2023, 24(1), 254; https://doi.org/10.3390/ijms24010254 - 23 Dec 2022
Viewed by 1298
Abstract
Bone marrow adiposity is a complication in osteoporotic patients. It is a result of the imbalance between adipogenic and osteogenic differentiation of bone marrow cells. Phytochemicals can alleviate osteoporotic complications by hindering bone loss and decreasing bone marrow adiposity. Corydalis heterocarpa is a [...] Read more.
Bone marrow adiposity is a complication in osteoporotic patients. It is a result of the imbalance between adipogenic and osteogenic differentiation of bone marrow cells. Phytochemicals can alleviate osteoporotic complications by hindering bone loss and decreasing bone marrow adiposity. Corydalis heterocarpa is a biennial halophyte with reported bioactivities, and it is a source of different coumarin derivatives. Libanoridin is a coumarin isolated from C. heterocarpa, and the effect of libanoridin on adipogenic differentiation of human bone marrow-derived mesenchymal stromal cells (hBM-MSCs) was evaluated in the present study. Cells were induced to undergo adipogenesis, and their intracellular lipid accumulation and expression of adipogenic markers were observed under libanoridin treatment. Results showed that 10 μM libanoridin-treated adipocytes accumulated 44.94% less lipid compared to untreated adipocytes. In addition, mRNA levels of PPARγ, C/EBPα, and SREBP1c were dose-dependently suppressed with libanoridin treatment, whereas only protein levels of PPARγ were decreased in the presence of libanoridin. Fluorescence staining of adipocytes also revealed that cells treated with 10 μM libanoridin expressed less PPARγ compared to untreated adipocytes. Protein levels of perilipin and leptin, markers of mature adipocytes, were also suppressed in adipocytes treated with 10 μM libanoridin. Analysis of MAPK phosphorylation levels showed that treatment with libanoridin inhibited the activation of p38 and JNK MAPKs observed by decreased levels of phosphorylated p38 and JNK protein. It was suggested that libanoridin inhibited adipogenic differentiation of hBM-MSCs via suppressing MAPK-mediated PPARγ signaling. Future studies revealing the anti-adipogenic effects of libanoridin in vivo and elucidating its action mechanism will pave the way for libanoridin to be utilized as a nutraceutical with anti-osteoporotic properties. Full article
(This article belongs to the Special Issue Recent Research in Primary Osteoporosis: From a Bone Marrow Adiposity Perspective)
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