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Diabetes is associated with significantly accelerated rates of several debilitating microvascular complications such as nephropathy, retinopathy, and neuropathy, and macrovascular complications such as atherosclerosis and stroke. While several studies have been devoted to the evaluation of genetic factors related to type 1 and type 2 diabetes and associated complications, much less is known about epigenetic changes that occur without alterations in the DNA sequence. Environmental factors and nutrition have been implicated in diabetes and can also affect epigenetic states. Exciting research has shown that epigenetic changes in chromatin can affect gene transcription in response to environmental stimuli, and changes in key chromatin histone methylation patterns have been noted under diabetic conditions. Reports also suggest that epigenetics may be involved in the phenomenon of metabolic memory observed in clinic trials and animal studies. Further exploration into epigenetic mechanisms can yield new insights into the pathogenesis of diabetes and its complications and uncover potential therapeutic targets and treatment options to prevent the continued development of diabetic complications even after glucose control has been achieved. [ABSTRACT FROM AUTHOR]

The article provides information on the aberrant epigenetic chromatin and the underlying mechanism for the persistent dysfunctional behavior of the diabetic cells. The role of chromatin immunoprecipitation assays involving active gene expression is discussed. Accordingly, protein levels of lysine-specific demethylase1 (LSD1) were reduced in the vascular smooth muscle cells (VSMC). Furthermore, the result of the study shows the functional roles of LSD1 and H3K4 methylation in inflammation.