Redox Homeostasis in Bone Health

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 5395

Special Issue Editors

Orthopaedic Institute, Medical College, Soochow University, Suzhou 215000, China
Interests: antioxidant functions; redox balance; bone metabolism; osteoporosis; intervertebral disc degeneration
B CUBE Center for Molecular Bioengineering, Technische Universität Dresden, 01307 Dresden, Germany
Interests: extracellular matrix; tissue engineering; scaffold

Special Issue Information

Dear Colleagues,

Bones play pivotal roles in the human body by providing structure, protecting organs, anchoring muscles, and storing calcium. Bone remodeling occurs continuously as evidenced by new bone formation coupled with old bone resorption. Bone tissue injury can initiate a variety of bone-related diseases, e.g., osteoporosis (OP) and osteoarthritis (OA). Therefore, protecting bone health is essential for human health.

Redox homeostasis, or redox signaling, helps maintain a normal physiological steady state. Inharmonic oxidative stress and antioxidant properties can trigger over-production of reactive oxygen species (ROS), leading to a series of cellular dysfunctions. Accumulated damage from mitochondrial ROS or endoplasmic reticulum (ER) stress is believed to be a major contributor to bone metabolism imbalance.

This Special Issue aims to provide a broad and updated overview of the involvement of redox homeostasis in bone health. An understanding of the interaction between oxidative stress and bone health, and their role in bone-related diseases, e.g., OA, OP, intervertebral disc degeneration (IVDD), etc., will aid the development of strategies for combating these pathological conditions. Original research and review articles are welcome.

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning redox homeostasis in bone metabolism. Potential topics include, but are not limited to, the following:

  • Sources and regulation of ROS in bone-related diseases;
  • Mechanisms of oxidative-stress-mediated signaling in bone health;
  • Interaction between ROS production, mitochondrial functions, and ER stress;
  • Roles of antioxidants in the treatment of bone dysfunction and bone-related diseases;
  • New strategies to interfere with oxidative stress and antioxidant strategies.

We look forward to your contributions.

Dr. Fan He
Dr. Yong Xu
Guest Editors

Manuscript Submission Information

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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. Antioxidants 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 2900 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

  • redox homeostasis
  • bone metabolism
  • bone disease
  • oxidative stress
  • antioxidant enzymes
  • mitochondrial ROS

Published Papers (2 papers)

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Research

18 pages, 4845 KiB  
Article
Blocking TRPV4 Ameliorates Osteoarthritis by Inhibiting M1 Macrophage Polarization via the ROS/NLRP3 Signaling Pathway
by Heng Sun, Ziying Sun, Xingquan Xu, Zhongyang Lv, Jiawei Li, Rui Wu, Yuxiang Fei, Guihua Tan, Zizheng Liu, Yuan Liu and Dongquan Shi
Antioxidants 2022, 11(12), 2315; https://doi.org/10.3390/antiox11122315 - 23 Nov 2022
Cited by 14 | Viewed by 2897
Abstract
Osteoarthritis (OA) is a low-level inflammatory disease in which synovial macrophage M1 polarization exacerbates the progression of synovitis and OA. Notedly, the ROS (reactive oxygen species) level in macrophages is intimately implicated in macrophage M1 polarization. TRPV4 (transient receptor potential channel subfamily V [...] Read more.
Osteoarthritis (OA) is a low-level inflammatory disease in which synovial macrophage M1 polarization exacerbates the progression of synovitis and OA. Notedly, the ROS (reactive oxygen species) level in macrophages is intimately implicated in macrophage M1 polarization. TRPV4 (transient receptor potential channel subfamily V member 4), as an ion channel, plays a pivotal role in oxidative stress and inflammation. In this study, we investigated the role of TRPV4 in OA progression and M1 macrophage polarization. Male adult Sprague–Dawley (SD) rats underwent a medial meniscus radial transection operation to create an OA model in vivo and RAW 264.7 cells were intervened with 100 ng/mL LPS (lipopolysaccharide) to induce M1-polarized macrophages in vitro. We demonstrated that the infiltration of M1 synovial macrophages and the expression of TRPV4 were increased significantly in OA synovium. In addition, intra-articular injection of HC067074 (a specific inhibitor of TRPV4) alleviated the progression of rat OA and significantly decreased synovial macrophage M1 polarization. Further mechanisms suggested that ROS production by M1 macrophages was decreased after TRPV4 inhibition. In addition, NLRP3 (pyrin domain containing protein 3) as a downstream effector of ROS in M1-polarized macrophage, was significantly suppressed following TRPV4 inhibition. In conclusion, this study discovered that inhibition of TRPV4 delays OA progression by inhibiting M1 synovial macrophage polarization through the ROS/NLRP3 pathway. Full article
(This article belongs to the Special Issue Redox Homeostasis in Bone Health)
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16 pages, 3624 KiB  
Article
Hedgehog Signalling Contributes to Trauma-Induced Tendon Heterotopic Ossification and Regulates Osteogenesis through Antioxidant Pathway in Tendon-Derived Stem Cells
by Guanzhi Li, Ye Deng, Kaiqun Li, Yuchen Liu, Ling Wang, Zhiyong Wu, Chao Chen, Kairui Zhang and Bin Yu
Antioxidants 2022, 11(11), 2265; https://doi.org/10.3390/antiox11112265 - 16 Nov 2022
Cited by 5 | Viewed by 1783
Abstract
Heterotopic ossification (HO) is defined as the generation of pathological ectopic bony structures in soft tissues, but the molecular mechanisms of tendon HO are not fully revealed. Hedgehog (Hh) signalling is reportedly critical in hereditary HO. Our study focuses on the role of [...] Read more.
Heterotopic ossification (HO) is defined as the generation of pathological ectopic bony structures in soft tissues, but the molecular mechanisms of tendon HO are not fully revealed. Hedgehog (Hh) signalling is reportedly critical in hereditary HO. Our study focuses on the role of Hh signalling in the formation of trauma-induced tendon ossification. In this study, samples of healthy tendons and injured tendons from C57BL/6J female mice at 1, 4, 7, and 10 weeks after Achilles tenotomy were collected for quantitative real-time polymerase chain reaction (qRT–PCR) and immunohistochemical analysis (IHC). At 1, 4, 7, and 10 weeks postinjury, tendon samples from the mice administered with vehicle, GANT58 (a GLI antagonist), or SAG (a smoothened agonist) were harvested for micro-CT, histological staining, qRT–PCR, and IHC. Rat tendon-derived stem cells (TDSCs) treated with vehicle, GANT58, or SAG were used to induce osteogenic and chondrogenic differentiation in vitro for qRT–PCR, alkaline phosphatase staining, Alcian blue staining, and reactive oxygen species (ROS) levels measurement. We found that Hh signalling is remarkably activated during the formation of trauma-induced tendon ossification in the model of Achilles tenotomy. The in vitro and in vivo assays both confirm that downregulation of Hh signalling significantly suppresses osteogenesis and chondrogenesis to inhibit tendon ossification, while upregulation of Hh signalling promotes this process. Under osteogenic induction, Hh signalling regulates antioxidant pathway and affects ROS generation of TDSCs. Collectively, Hh signalling contributes to trauma-induced tendon ossification and affects ROS generation through antioxidant pathway in osteogenic differentiation of TDSCs, indicating that targeting Hh signalling by GANT58 may be a potential treatment for trauma-induced tendon ossification. Full article
(This article belongs to the Special Issue Redox Homeostasis in Bone Health)
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