Abstract
Osteoarthritis (OA) is the most common type of arthritis, a disease that affects the entire joint. The relative involvement of each tissue, and their interactions, add to the complexity of OA, hampering our understanding of the underlying molecular mechanisms, and the generation of a disease modifying therapy. The synovium is essential in maintaining joint homeostasis, and pathologies associated with the synovium contribute to joint destruction, pain and stiffness in OA. MicroRNAs (miRNAs) are post-transcriptional regulators dysregulated in OA tissues including the synovium. MiRNAs are important contributors to OA synovial changes that have the potential to improve our understanding of OA and to act as novel therapeutic targets. The purpose of this review is to summarize and integrate current published literature investigating the roles that miRNAs play in OA-related synovial pathologies including inflammation, matrix deposition and cell proliferation.
Highlights
Osteoarthritis (OA) is the most common chronic debilitating disease imposing a significant socioeconomic burden and affecting the quality of life of millions of people worldwide [1]
The complex network of miRNAs that regulate the pathophysiology of cartilage degeneration during OA has been previously reviewed [6]; very little is known regarding the role of miRNAs in regulating synovial gene expression during OA
We summarize the contributions of the synovium to OA pathology and how focusing on the role of miRNAs in regulating the activity of fibroblast-like synoviocytes (FLS) warrants further study to further elucidate mechanisms contributing to OA pathologies
Summary
Osteoarthritis (OA) is the most common chronic debilitating disease imposing a significant socioeconomic burden and affecting the quality of life of millions of people worldwide [1]. OA affects the whole joint and involves progressive articular cartilage degradation, subchondral bone remodeling, ectopic bone formation, ligament degeneration, menisci degradation, and synovial inflammation and hypertrophy [2]. OA alters the homeostatic functions of cells residing in the synovium, but we are only starting to elucidate the underlying gene expression and regulatory mechanisms responsible, and how these changes contribute to disease progression. The complex network of miRNAs that regulate the pathophysiology of cartilage degeneration during OA has been previously reviewed [6]; very little is known regarding the role of miRNAs in regulating synovial gene expression during OA. We summarize the contributions of the synovium to OA pathology and how focusing on the role of miRNAs in regulating the activity of fibroblast-like synoviocytes (FLS) warrants further study to further elucidate mechanisms contributing to OA pathologies
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