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Redox Signaling and Oxidative Stress in Bone Health and Disease
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Redox Signaling and Oxidative Stress in Bone Health and Disease

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 (30 November 2020) | Viewed by 6970

Special Issue Editor

Dr. Ha-Neui Kim

E-Mail Website
Guest Editor
Center for Musculoskeletal Disease Research and Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Little Rock, AR 72205-7199, USA
Interests: osteoclasts; osteoblasts; osteocytes; mitochondrial quality control; osteoporosis; aging; cellular senescence; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Balance between bone resorption and formation is essential to maintain bone homeostasis. However, physiological or pathological changes, such as aging or inflammation, can lead to both an increase in osteoclast and a decrease in osteoblast numbers, and eventually cause skeletal diseases. Thus, a better understanding the cellular and molecular mechanism(s) involved in the differentiation and activation of skeletal cells as well as chondrocytes is important for the development of novel therapies to treat skeletal diseases.

There is growing evidence that reactive oxygen species (ROS) play an important role in physiological intracellular signalling by triggering proliferation and survival in many different types of cells, including osteoclasts, osteoblasts, osteocytes, and chondrocytes. Mitochondrial oxidative phosphorylation produces ROS as by-products, which can be important signaling molecules but damage cells and contribute to disease and aging when they become excessive.

We invite researchers to submit original research and review articles covering significant developments in the mitochondrial function and oxidative stress of bone cells, as well as novel medicines or strategies that hold promise in the prevention and/or treatment of skeletal diseases. In particular, we welcome research covering novel molecular mechanism, new tools on bone research, or any animal studies with clinical relevance.

Dr. Ha-Neui Kim
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

  • osteoclast
  • osteoblast
  • osteocyte
  • chondrocyte
  • ROS
  • mitochondria
  • skeletal diseases
  • aging

Published Papers (2 papers)

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Research

15 pages, 3316 KiB  
Article
Inhibitory Effect of (2R)-4-(4-hydroxyphenyl)-2-butanol 2-O-β-d-apiofuranosyl-(1→6)-β-d-glucopyranoside on RANKL-Induced Osteoclast Differentiation and ROS Generation in Macrophages
by Eun-Nam Kim, Ga-Ram Kim, Jae Sik Yu, Ki Hyun Kim and Gil-Saeng Jeong
Int. J. Mol. Sci. 2021, 22(1), 222; https://doi.org/10.3390/ijms22010222 - 28 Dec 2020
Cited by 9 | Viewed by 2155
Abstract
In bone homeostasis, bone loss due to excessive osteoclasts and inflammation or osteolysis in the bone formation process cause bone diseases such as osteoporosis. Suppressing the accompanying oxidative stress such as ROS in this process is an important treatment strategy for bone disease. [...] Read more.
In bone homeostasis, bone loss due to excessive osteoclasts and inflammation or osteolysis in the bone formation process cause bone diseases such as osteoporosis. Suppressing the accompanying oxidative stress such as ROS in this process is an important treatment strategy for bone disease. Therefore, in this study, the effect of (2R)-4-(4-hydroxyphenyl)-2-butanol 2-O-β-d-apiofuranosyl-(1→6)-β-d-glucopyranoside (BAG), an arylbutanoid glycoside isolated from Betula platyphylla var. japonica was investigated in RANKL-induced RAW264.7 cells and LPS-stimulated MC3E3-T1 cells. BAG inhibited the activity of TRAP, an important marker of osteoclast differentiation and F-actin ring formation, which has osteospecific structure. In addition, the protein and gene levels were suppressed of integrin β3 and CCL4, which play an important role in the osteoclast-induced bone resorption and migration of osteoclasts, and inhibited the production of ROS and restored the expression of antioxidant enzymes such as SOD and CAT lost by RANKL. The inhibitory effect of BAG on osteoclast differentiation and ROS production appears to be due to the inhibition of MAPKs phosphorylation and NF-κβ translocation, which play a major role in osteoclast differentiation. In addition, BAG inhibited ROS generated by LPS and effectively restores the mineralization of lost osteoblasts, thereby showing the effect of bone formation in the inflammatory situation accompanying bone loss by excessive osteoclasts, suggesting its potential as a new natural product-derived bone disease treatment. Full article
(This article belongs to the Special Issue Redox Signaling and Oxidative Stress in Bone Health and Disease)
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19 pages, 13043 KiB  
Article
Intraarticular Administration Effect of Hydrogen Sulfide on an In Vivo Rat Model of Osteoarthritis
by Carlos Vaamonde-García, Elena F. Burguera, Ángela Vela-Anero, Tamara Hermida-Gómez, Purificación Filgueira-Fernández, Jennifer A. Fernández-Rodríguez, Rosa Meijide-Faílde and Francisco J. Blanco
Int. J. Mol. Sci. 2020, 21(19), 7421; https://doi.org/10.3390/ijms21197421 - 8 Oct 2020
Cited by 16 | Viewed by 4391
Abstract
Osteoarthritis (OA) is the most common articular chronic disease. However, its current treatment is limited and mostly symptomatic. Hydrogen sulfide (H2S) is an endogenous gas with recognized physiological activities. The purpose here was to evaluate the effects of the intraarticular administration [...] Read more.
Osteoarthritis (OA) is the most common articular chronic disease. However, its current treatment is limited and mostly symptomatic. Hydrogen sulfide (H2S) is an endogenous gas with recognized physiological activities. The purpose here was to evaluate the effects of the intraarticular administration of a slow-releasing H2S compound (GYY-4137) on an OA experimental model. OA was induced in Wistar rats by the transection of medial collateral ligament and the removal of the medial meniscus of the left joint. The animals were randomized into three groups: non-treated and intraarticularly injected with saline or GYY-4137. Joint destabilization induced articular thickening (≈5% increment), the loss of joint mobility and flexion (≈12-degree angle), and increased levels of pain (≈1.5 points on a scale of 0 to 3). Animals treated with GYY-4137 presented improved motor function of the joint, as well as lower pain levels (≈75% recovery). We also observed that cartilage deterioration was attenuated in the GYY-4137 group (≈30% compared with the saline group). Likewise, these animals showed a reduced presence of pro-inflammatory mediators (cyclooxygenase-2, inducible nitric oxide synthase, and metalloproteinase-13) and lower oxidative damage in the cartilage. The increment of the nuclear factor-erythroid 2-related factor 2 (Nrf-2) levels and Nrf-2-regulated gene expression (≈30%) in the GYY-4137 group seem to be underlying its chondroprotective effects. Our results suggest the beneficial impact of the intraarticular administration of H2S on experimental OA, showing a reduced cartilage destruction and oxidative damage, and supporting the use of slow H2S-producing molecules as a complementary treatment in OA. Full article
(This article belongs to the Special Issue Redox Signaling and Oxidative Stress in Bone Health and Disease)
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