Abstract
Gout is a form of arthritis, resulting from an inflammatory reaction to the deposition of monosodium urate (MSU) crystals in the synovial fluid of the joint space. It is characterised by periods of acute inflammation in the affected joint, or joints (known as gout flares), separated by asymptomatic periods. There seems to be substantial overlap between environmental triggers of gout flares and common environmental modifiers (diet, pharmaceuticals, and stress) of epigenetic markers (DNA methylation, histone modifications, and ncRNA). Very few studies have looked at whether environment is influencing gout through epigenetic mechanisms. The pathogenesis of gouty inflammation is well understood but understanding the variation of response to hyperuricaemia in terms of gout flare initiation is less well known. In this review, we will examine the potential of epigenomics in understanding how gout flares may occur, both in terms of development of hyperuricaemia and the inflammatory response. Looking at the epigenome and its intersection with lifestyle could help identify new targets and strategies for effective management of gout flares.
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