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Metabolites
Special Issues
Metabolomics in Bone and Joint
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Metabolomics in Bone and Joint

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Advances in Metabolomics".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 6009

Special Issue Editor

Prof. Takeshi Miyamoto

E-Mail Website
Guest Editor
Department of Orthopedic Surgery, Keio university School of Medicine, Tokyo 160-8582, Japan
Interests: bone metabolism; osteoporosis; osteoarthritis; rheumatoid arthritis; orthopedic surgery

Special Issue Information

Dear Colleagues,

Bone is a highly metabolic organ, and its homeostasis is regulated in a remodeling process. During this process, levels of various metabolites are changed, and some are useful to in the diagnosis of or as markers of bone diseases such as osteoporosis. However, physiological and pathological metabolomic changes in bones remain to be elucidated, and the metabolites to evaluate or predict bone diseases are still needed. Meanwhile, articular cartilage tissues are metabolically silent, and the metabolomic changes during their physiological or disease state (e.g., osteoarthritis) have not been fully clarified. Furthermore, metabolomic approaches to inflammatory joint diseases such as rheumatoid arthritis are still needed to characterize the diseases, since these diseases are quite heterogeneous.

This Special Issue of Metabolites, "Metabolomics in Bone and Joint" will be dedicated to publishing current advances in our understanding of metabolic regulations and metabolic networks in bone and joint in physiological and pathological states, and to characterize specific metabolites or molecules regulating metabolism in these organs.

Prof. Dr. Takeshi Miyamoto
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. Metabolites is an international peer-reviewed open access monthly 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

  • bone
  • joint
  • cartilage
  • chondrocyte
  • rheumatoid arthritis
  • remodeling
  • osteoclasts
  • osteocytes
  • osteoblasts

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Published Papers (2 papers)

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Research

11 pages, 2631 KiB  
Article
Analysis of Serum Proteome after Treatment of Osteoporosis with Anabolic or Antiresorptive Drugs
by Alvaro del Real, Sergio Ciordia, Carolina Sañudo, Carmen Garcia-Ibarbia, Adriel Roa-Bautista, Javier G. Ocejo-Viñals, Fernando Corrales and Jose A. Riancho
Metabolites 2022, 12(5), 399; https://doi.org/10.3390/metabo12050399 - 28 Apr 2022
Cited by 4 | Viewed by 2219
Abstract
The aim of the study was to explore new markers in serum proteome associated with the response to antiosteoporosis drugs, namely teriparatide and denosumab. We obtained serum samples from 14 patients with osteoporosis, both at baseline and after 6 months of treatment with [...] Read more.
The aim of the study was to explore new markers in serum proteome associated with the response to antiosteoporosis drugs, namely teriparatide and denosumab. We obtained serum samples from 14 patients with osteoporosis, both at baseline and after 6 months of treatment with teriparatide (n = 10) or denosumab (n = 4). Samples were analyzed by nanoliquid chromatography coupled to high-resolution mass spectrometry on a QTOF 5600 (SCIEX) apparatus. The spectrometry data were analyzed with Mascot against the UniProtKB base and then several quality-control filters were applied for the identification of peptides (false discovery rate, FDR q < 0.02) and their quantification (FDR q < 0.05). In the group treated with teriparatide, 28 proteins were identified with significant differences before and after treatment. A pathway analysis by using the Reactome database revealed significant enrichment in the Insulin Like Growth Factor 1 (IGF-I) (FDR q 4 × 10−2) and innate immune system (FDR q 2 × 10−3) pathways. Among patients treated with denosumab, we observed significant differences in the levels of 10 proteins, which were also enriched in the pathways related to the innate immune system (FDR q 3 × 10−2). These results suggest that the innate immune system may be involved in the response to antiosteoporosis drugs. Full article
(This article belongs to the Special Issue Metabolomics in Bone and Joint)
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12 pages, 2102 KiB  
Article
Hao1 Is Not a Pathogenic Factor for Ectopic Ossifications but Functions to Regulate the TCA Cycle In Vivo
by Atsushi Kimura, Akiyoshi Hirayama, Tatsuaki Matsumoto, Yuiko Sato, Tami Kobayashi, Satsuki Ikeda, Midori Maruyama, Mari Kaneko, Mayo Shigeta, Eri Ito, Tomoya Soma, Kana Miyamoto, Tomoyoshi Soga, Masaru Tomita, Akihito Oya, Morio Matsumoto, Masaya Nakamura, Arihiko Kanaji and Takeshi Miyamoto
Metabolites 2022, 12(1), 82; https://doi.org/10.3390/metabo12010082 - 15 Jan 2022
Cited by 4 | Viewed by 3104
Abstract
Ossification of the posterior longitudinal ligament (OPLL), a disease characterized by the ectopic ossification of a spinal ligament, promotes neurological disorders associated with spinal canal stenosis. While blocking ectopic ossification is mandatory to prevent OPLL development and progression, the mechanisms underlying the condition [...] Read more.
Ossification of the posterior longitudinal ligament (OPLL), a disease characterized by the ectopic ossification of a spinal ligament, promotes neurological disorders associated with spinal canal stenosis. While blocking ectopic ossification is mandatory to prevent OPLL development and progression, the mechanisms underlying the condition remain unknown. Here we show that expression of hydroxyacid oxidase 1 (Hao1), a gene identified in a previous genome-wide association study (GWAS) as an OPLL-associated candidate gene, specifically and significantly decreased in fibroblasts during osteoblast differentiation. We then newly established Hao1-deficient mice by generating Hao1-flox mice and crossing them with CAG-Cre mice to yield global Hao1-knockout (CAG-Cre/Hao1flox/flox; Hao1 KO) animals. Hao1 KO mice were born normally and exhibited no obvious phenotypes, including growth retardation. Moreover, Hao1 KO mice did not exhibit ectopic ossification or calcification. However, urinary levels of some metabolites of the tricarboxylic acid (TCA) cycle were significantly lower in Hao1 KO compared to control mice based on comprehensive metabolomic analysis. Our data indicate that Hao1 loss does not promote ectopic ossification, but rather that Hao1 functions to regulate the TCA cycle in vivo. Full article
(This article belongs to the Special Issue Metabolomics in Bone and Joint)
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