Abstract
Osteoarthritis (OA) is a common degenerative disease characterized by the destruction of articular cartilage and chronic inflammation of surrounding tissues. Matrix metalloproteinase-13 (MMP-13) is the primary MMP involved in cartilage degradation through its particular ability to cleave type II collagen. Hence, it is an attractive target for the treatment of OA. However, the detailed molecular mechanisms of OA initiation and progression remain elusive, and, currently, there are no interventions available to restore degraded cartilage. This review fully illustrates the involvement of MMP-13 in the initiation and progression of OA through the regulation of MMP-13 activity at the molecular and epigenetic levels, as well as the strategies that have been employed against MMP-13. The aim of this review is to identify MMP-13 as an attractive target for inhibitor development in the treatment of OA.
Highlights
Osteoarthritis (OA) is one of the most common degenerative joint diseases primarily among the elderly who exhibit typical clinical symptoms such as joint pain, swelling, stiffness, and restricted movement
Transforming growth factor-β (TGF-β) sub-pathway have a protective function in articular cartilage, but the expected role is altered in human OA cartilage because the expression levels of TGF-β isoforms are negatively correlated with the expressions of main proteins in human cartilage, i.e., type II collagen and aggrecan [68]
We discuss the recent advances made in understanding the role of Matrix metalloproteinase-13 (MMP-13) in OA development and the therapeutic potential of MMP-13 inhibition in that condition
Summary
Osteoarthritis (OA) is one of the most common degenerative joint diseases primarily among the elderly who exhibit typical clinical symptoms such as joint pain, swelling, stiffness, and restricted movement. Other novel treatments have been extensively studied, like low-dose radiation [25] and intra-articular injection, including agonist for the transient receptor potential cation channel subfamily V member 1 (e.g., Capsaicin) [26], IL-1α/β dual variable domain immunoglobulin (e.g., Lutikizumab) [27], a humanized monoclonal antibody (e.g., Galcanezumab) [28], and regenerative medicine (e.g., platelet-rich plasma or mesenchymal stem cell) [29,30]. These treatments are limited to clinical trials with no or inadequate efficacy. Additional information retrieval was made when it comes to specific problems
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