作者: Wouter Hollander , Ingrid Meulenbelt
DOI: 10.2174/1389202916666150817212711
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摘要: Osteoarthritis (OA) is a prevalent disease of articular joints and primarily characterized by degradation calcification cartilage. Presently, no effective treatment other than pain relief exists patients ultimately need to undergo replacement surgery the affected joint. During progression chondrocytes, single cell type present in cartilage, show altered transcriptional profiles phenotypic changes that resemble terminal differentiation route apparent growth plate chondrocytes. Hence, given its prominent function both regulating gene expression maintaining cellular phenotypes, DNA methylation CpG dinucleotides intensively studied context OA. An increasing number studies have been published employed targeted approach on genes known play role OA pathophysiology. As such, it has become clear responsive seem mediate associated aberrant expression. Furthermore, established susceptibility alleles such as GDF5 DIO2 appear confer risk via respective pathophysiological changes. In more recent years, genome wide profiling cartilage emerged powerful tool address epigenetic their entirety, which resulted identification putative patient subgroups well generic pathways.