Epigenetic mechanisms and non-coding RNAs in osteoarthritis

MJ Barter, DA Young - Current rheumatology reports, 2013 - Springer
Current rheumatology reports, 2013Springer
Osteoarthritis (OA) is a disease typified by the loss of cartilage, the normal integrity of which
is maintained by the resident cell, the chondrocyte. Alterations in chondrocyte gene
expression with age, injury, loading or predisposing genetics, underpin OA cartilage loss.
Cell-and tissue-specific gene expression is determined by epigenetic mechanisms,
including DNA methylation, chromatin modifications and non-coding RNAs, including
microRNAs and long-non-coding RNAs. A number of epigenetic changes have been …
Abstract
Osteoarthritis (OA) is a disease typified by the loss of cartilage, the normal integrity of which is maintained by the resident cell, the chondrocyte. Alterations in chondrocyte gene expression with age, injury, loading or predisposing genetics, underpin OA cartilage loss. Cell- and tissue-specific gene expression is determined by epigenetic mechanisms, including DNA methylation, chromatin modifications and non-coding RNAs, including microRNAs and long-non-coding RNAs. A number of epigenetic changes have been identified between OA and normal cartilage, and the enzymes which impart the epigenetic code are increasingly seen as important players in a number of pathologies, including OA. Here, we will describe current and potential new epigenetic studies that are likely to reveal novel aspects of chondrocyte and cartilage biology and potentially help sub-characterise OA phenotypes. Importantly, many of these epigenetic modifiers or non-coding RNAs are proposed drug targets and could represent a therapeutic opportunity for this currently untreatable disease.
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