Submit to Antioxidants Review for Antioxidants Propose a Special Issue

Journal Browser

ROS/Oxidative Stress Signaling in Osteoarthritis

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Published Papers

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 (20 August 2022) | Viewed by 11382

Share This Special Issue

Special Issue Editor

Prof. Dr. Yonggeun Hong

E-Mail Website
Guest Editor

Department of Physical Therapy, College of Healthcare Medical Science & Engineering, Biohealth Products Research Center (BPRC), u-Healthcare & Anti-aging Research Center (u-HARC), Inje University, Gimahe, Korea
Interests: regulation of biological clock; degenerative neural diseases; regulation of clock-clontrolled genes by melatonin; anti-aging process in neural tissue by melatonin; melatonin effect in ASD during developmental stages
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Osteoarthritis (OA) is a complex joint disorder of multifactorial etiology with increasing prevalence due to the aging of the populations. The driving force behind OA pathogenesis includes oxidative stress and the overproduction of reactive oxygen species (ROS), which regulate intracellular signaling processes, chondrocyte senescence and programmed cell death, extracellular matrix synthesis and deterioration along with synovial inflammation and dysfunction of the subchondral bone. Since disease-modifying drugs to mitigate OA pathogenesis are rare, targeting the intricate oxidative stress/ROS signaling pathways would offer a valuable perspective to investigate the potential therapeutic strategies in OA pathogenesis.

Currently, many scientists have been investigating the underlying molecular mechanisms of ROS production and their action in OA progression, while other researchers have been developing new therapeutic strategies to inhibit the development of OA by regulating oxidative stress.

We encourage scientists to contribute with original articles describing novel mechanisms by which oxidative stress contributes to the development of OA as well as new therapeutic strategies to treat or prevent this pathological status in which oxidative stress might be involved. Narrative and systematic reviews that summarize recent findings in both basic and clinical research and discuss current outcome are also welcome.

Prof. Dr. Yonggeun Hong
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. 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

osteoarthritis
reactive oxygen species
oxidative stress
antioxidants
anabolic/catabolic effects
natural compounds

Published Papers (4 papers)

Download All Papers

Research

Jump to: Review

26 pages, 18005 KiB

Open AccessArticle

β Boswellic Acid Blocks Articular Innate Immune Responses: An In Silico and In Vitro Approach to Traditional Medicine

by Eloi Franco-Trepat, Ana Alonso-Pérez, María Guillán-Fresco, Miriam López-Fagúndez, Andrés Pazos-Pérez, Antía Crespo-Golmar, Susana Belén Bravo, Verónica López-López, Alberto Jorge-Mora, José P. Cerón-Carrasco, Ana Lois Iglesias and Rodolfo Gómez

Antioxidants 2023, 12(2), 371; https://doi.org/10.3390/antiox12020371 - 03 Feb 2023

Cited by 4 | Viewed by 2128

Abstract

Osteoarthritis (OA) is hallmarked as a silent progressive rheumatic disease of the whole joint. The accumulation of inflammatory and catabolic factors such as IL6, TNFα, and COX2 drives the OA pathophysiology into cartilage degradation, synovia inflammation, and bone destruction. There is no clinical available OA treatment. Although traditional ayurvedic medicine has been using Boswellia serrata extracts (BSE) as an antirheumatic treatment for a millennium, none of the BSE components have been clinically approved. Recently, β boswellic acid (BBA) has been shown to reduce in vivo OA-cartilage loss through an unknown mechanism. We used computational pharmacology, proteomics, transcriptomics, and metabolomics to present solid evidence of BBA therapeutic properties in mouse and primary human OA joint cells. Specifically, BBA binds to the innate immune receptor Toll-like Receptor 4 (TLR4) complex and inhibits both TLR4 and Interleukin 1 Receptor (IL1R) signaling in OA chondrocytes, osteoblasts, and synoviocytes. Moreover, BBA inhibition of TLR4/IL1R downregulated reactive oxygen species (ROS) synthesis and MAPK p38/NFκB, NLRP3, IFNαβ, TNF, and ECM-related pathways. Altogether, we present a solid bulk of evidence that BBA blocks OA innate immune responses and could be transferred into the clinic as an alimentary supplement or as a therapeutic tool after clinical trial evaluations. Full article

(This article belongs to the Special Issue ROS/Oxidative Stress Signaling in Osteoarthritis)

► Show Figures

Graphical abstract

16 pages, 3284 KiB

Open AccessArticle

Characterization of Non-Invasively Induced Post-Traumatic Osteoarthritis in Mice

by Fazal-Ur-Rehman Bhatti, Yong-Hoon Jeong, Do-Gyoon Kim, Ae-Kyung Yi, David D. Brand, Karen A. Hasty and Hongsik Cho

Antioxidants 2022, 11(9), 1783; https://doi.org/10.3390/antiox11091783 - 09 Sep 2022

Cited by 5 | Viewed by 1902

Abstract

The pathophysiology of post-traumatic arthritis (PTOA) is not fully understood. This study used non-invasive repetitive mechanical loading (ML) mouse models to study biochemical, biomechanical, and pain-related behavioral changes induced in mice. Mouse models reflected the effects of the early stages of PTOA in humans. For the PTOA model, cyclic comprehensive loading (9N) was applied to each mouse’s left knee joint. ML-induced biochemical and molecular changes were analyzed after loading completion. Cartilage samples were examined using gene expression analysis. Tissue sections were used in subsequent OA severity scoring. Biomechanical features and pain-related behavior were studied after 24 h and three weeks post-ML sessions to examine the development of PTOA. The loaded left knee joint showed a greater ROS/RNS signal than the right knee, which was not loaded. There was a significant increase in cartilage damage and MMP activity in the mechanically loaded joints relative to non-loaded control knee joints. Similarly, we found a difference in the viscoelastic tangent, which highlights significant changes in mechanical properties. Biochemical analyses revealed significant increases in total NO, caspase-3 activity, H₂O₂, and PGE2 levels. Gene expression analysis highlighted increased catabolism (MMP-13, IL-1β, TNF-α) with a concomitant decrease in anabolism (ACAN, COL2A1). Histopathology scores clearly indicated increases in OA progression and synovitis. The gait pattern was significantly altered, suggesting signs of joint damage. This study showed that biomechanical, biochemical, and behavioral characteristics of the murine PTOA groups are significantly different from the control group. These results confirm that the current mouse model can be considered for translational PTOA studies. Full article

(This article belongs to the Special Issue ROS/Oxidative Stress Signaling in Osteoarthritis)

► Show Figures

Figure 1

Review

Jump to: Research

29 pages, 2055 KiB

Open AccessReview

Natural Compounds Affecting Inflammatory Pathways of Osteoarthritis

by Yi Ting Lee, Mohd Heikal Mohd Yunus, Azizah Ugusman and Muhammad Dain Yazid

Antioxidants 2022, 11(9), 1722; https://doi.org/10.3390/antiox11091722 - 30 Aug 2022

Cited by 2 | Viewed by 3209

Abstract

Osteoarthritis (OA) is the most common type of arthritis and chronic joint disease, affecting more than 240 million people worldwide. Although there are numerous advances in using drugs in treating OA, the use of natural compounds has aroused much interest among researchers due to their safety margin. Recent discovery shows that natural compounds play an extensive role in the oxidative stress signaling pathway in treating OA. Thus, this review summarizes the commonly used natural compounds for treating OA focusing on the oxidative stress signaling pathway and its downstream mediators. Selected databases—such as Scopus, Web of Science, Nature, and PubMed—were used to search for potentially relevant articles. The search is limited to the last 15 years and the search was completed using the Boolean operator’s guideline using the keywords of natural product AND oxidative stress AND osteoarthritis OR natural extract AND ROS AND degenerative arthritis OR natural plant AND free radicals AND degenerative joint disease. In total, 37 articles were selected for further review. Different downstream mechanisms of oxidative stress involved in the usage of natural compounds for OA treatment and anabolic and catabolic effects of natural compounds that exhibit chondroprotective effects have been discussed with the evidence of in vitro and in vivo trials in this review. Full article

(This article belongs to the Special Issue ROS/Oxidative Stress Signaling in Osteoarthritis)

► Show Figures

Figure 1

22 pages, 1151 KiB

Open AccessReview

The Role Played by Ferroptosis in Osteoarthritis: Evidence Based on Iron Dyshomeostasis and Lipid Peroxidation

by Shaoyun Zhang, Jiawen Xu, Haibo Si, Yuangang Wu, Shengliang Zhou and Bin Shen

Antioxidants 2022, 11(9), 1668; https://doi.org/10.3390/antiox11091668 - 27 Aug 2022

Cited by 17 | Viewed by 3468

Abstract

Ferroptosis, a recently discovered regulated cell death modality, is characterised by iron-dependent accumulation of lipid hydroperoxides, which can reach lethal levels but can be specifically reversed by ferroptosis inhibitors. Osteoarthritis (OA), the most common degenerative joint disease, is characterised by a complex pathogenesis involving mechanical overload, increased inflammatory mediator levels, metabolic alterations, and cell senescence and death. Since iron accumulation and oxidative stress are the universal pathological features of OA, the role played by ferroptosis in OA has been extensively explored. Increasing evidence has shown that iron dyshomeostasis and lipid peroxidation are closely associated with OA pathogenesis. Therefore, in this review, we summarize recent evidence by focusing on ferroptotic mechanisms and the role played by ferroptosis in OA pathogenesis from the perspectives of clinical findings, animal models, and cell research. By summarizing recent research advances that characterize the relationship between ferroptosis and OA, we highlight avenues for further research and potential therapeutic targets. Full article

(This article belongs to the Special Issue ROS/Oxidative Stress Signaling in Osteoarthritis)

► Show Figures