To provide an overview of the literature describing the role of asporin, a small leucine-rich proteoglycan (SLRP), in osteoarthritis (OA).
A literature search was performed and reviewed using the narrative approach.
As a class I SLRP member, asporin, is distinct from other SLRPs. Accumulating evidence demonstrates the involvement of asporin in OA pathogenesis. Many human studies have been conducted to explore the association between the D-repeat polymorphisms and OA susceptibility, but these yield inconsistent results. Possible mechanisms for the involvement of asporin in OA pathology include its influence on TGF-β (transforming growth factor-β) signaling pathways and collagen mineralization. To date, no studies were found to use an asporin-deficient animal model that would help to understand disease mechanisms. Many issues must be addressed to clarify the link between asporin and OA to provide a novel therapeutic strategy for OA, perhaps through controlling and modifying the TGF-β-ECM system.
Studies examined demonstrate the involvement of asporin in OA pathogenesis, and possible mechanisms by which asporin may be involved in this process have been proposed. However, large-scale interracial studies should be conducted to investigate the association between asporin and OA, and further investigations are needed to obtain a better understanding of the disease mechanism, develop novel therapeutic strategies, and explore new approaches for diagnosis of OA.