Diabetic nephropathy (DN) belongs to debilitating microvascular complications of diabetes and is the leading cause of end-stage\nrenal diseases worldwide. Furthermore, outcomes from the DCCT/EDIC study showed that DN often persists and progresses\ndespite intensive glucose control in many diabetes patients, possibly as a result of prior episode of hyperglycemia, which is\ncalled ââ?¬Å?metabolic memory.ââ?¬Â The underlying mechanisms responsible for the development and progression of DN remain poorly\nunderstood. Activation of multiple signaling pathways and key transcription factors can lead to aberrant expression of DNrelated\npathologic genes in target renal cells. Increasing evidence suggests that epigenetic mechanisms in chromatin such as DNA\nmethylation, histone acetylation, and methylation can influence the pathophysiology of DN and metabolic memory. Exciting\nresearches from cell culture and experimental animals have shown that key histone methylation patterns and the related histone\nmethyltransferases and histone demethylases can play important roles in the regulation of inflammatory and profibrotic genes in\nrenal cells under diabetic conditions. Because histone methylation is dynamic and potentially reversible, it can provide a window of\nopportunity for the development of much-needed novel therapeutic potential for DN in the future. In this minireview, we discuss\nrecent advances in the field of histone methylation and its roles in the pathogenesis and progression of DN.
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