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Standardized Histomorphometric Evaluation of Osteoarthritis in a Surgical Mouse Model
Published on: May 6, 2020
HYBID in osteoarthritis: Potential target for disease progression
Shengyuan Zheng1, Senbo An2, Yan Luo3
1Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Clinical Medicine, Xiangya Medicine School, Central South University, Changsha, Hunan, China.
Insights
HYBID, a hyaluronan-degrading enzyme, is over-expressed in osteoarthritis, driving cartilage degeneration and joint inflammation. Targeting HYBID offers a novel therapeutic strategy for osteoarthritis treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Rheumatology
Background:
- HYBID (hyaluronan-degrading enzyme) is present in human cells and over-expressed in osteoarthritic chondrocytes and synoviocytes.
- Elevated HYBID levels correlate with cartilage degeneration and hyaluronic acid degradation in synovial fluid.
Purpose of the Study:
- To review the expression and function of HYBID in joints.
- To explore the potential of HYBID as a therapeutic target for osteoarthritis.
Main Methods:
- Literature review of existing research on HYBID in osteoarthritis.
- Analysis of HYBID's role in cartilage metabolism and signaling pathways.
Main Results:
- HYBID exacerbates osteoarthritis by degrading hyaluronic acid, affecting cartilage structure, and influencing inflammatory pathways.
- HYBID's degradation activity is independent of the HYALs/CD44 system.
- Degradation products of hyaluronic acid by HYBID may also promote disease pathways.
Conclusions:
- HYBID plays a significant role in the pathogenesis of osteoarthritis.
- Targeting HYBID presents a promising new avenue for osteoarthritis treatment.
Abstract:
HYBID is a new hyaluronan-degrading enzyme and exists in various cells of the human body. Recently, HYBID was found to over-express in the osteoarthritic chondrocytes and fibroblast-like synoviocytes. According to these researches, high level of HYBID is significantly correlated with cartilage degeneration in joints and hyaluronic acid degradation in synovial fluid. In addition, HYBID can affect inflammatory cytokine secretion, cartilage and synovium fibrosis, synovial hyperplasia via multiple signaling pathways, thereby exacerbating osteoarthritis. Based on the existing research of HYBID in osteoarthritis, HYBID can break the metabolic balance of HA in joints through the degradation ability independent of HYALs/CD44 system and furthermore affect cartilage structure and mechanotransduction of chondrocytes. In particular, in addition to HYBID itself being able to trigger some signaling pathways, we believe that low-molecular-weight hyaluronan produced by excess degradation can also stimulate some disease-promoting signaling pathways by replacing high-molecular-weight hyaluronan in joints. The specific role of HYBID in osteoarthritis is gradually revealed, and the discovery of HYBID raises the new way to treat osteoarthritis. In this review, the expression and basic functions of HYBID in joints were summarized, and reveal potential role of HYBID as a key target in treatment for osteoarthritis.
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