Epigenetic Mechanisms in Diabetic Kidney Disease

• Published in: Current diabetes reports 2016-03, Vol.16 (3), p.31-31, Article 31
• Main Author: Thomas, Merlin C.
• Format: Article
• Language: English
• Subjects: Animals; Diabetes; Diabetic Nephropathies - genetics; DNA Methylation; Epigenesis, Genetic; Humans; Hyperglycemia - complications; Hyperglycemia - genetics; Medicine; Medicine & Public Health; Microvascular Complications—Nephropathy (AP Maxwell; Risk Factors; RNA, Untranslated - genetics; Section Editor; Topical Collection on Microvascular Complications—Nephropathy
• ISSN: 1534-4827; 1539-0829
• DOI: 10.1007/s11892-016-0723-9

Progressive kidney disease is a common companion to both type 1 and type 2 diabetes. However, the majority of people with diabetes do not develop diabetic kidney disease. This may in part be explained by good control of glucose, blood pressure, obesity and other risk factors for kidney disease. It may also be partly due to their genetic makeup or ethnicity. However, the vast majority of the variability in incident nephropathy remains unaccounted for by conventional risk factors or genetics. Epigenetics has recently emerged as an increasingly powerful paradigm to understand and potentially explain complex non-Mendelian conditions—including diabetic kidney disease. Persistent epigenetic changes can be acquired during development or as adaptations to environmental exposure, including metabolic fluctuations associated with diabetes. These epigenetic modifications—including DNA methylation, histone modifications, non-coding RNAs and other changes in chromatin structure and function—individually and co-operatively act to register, store, retain and recall past experiences in a way to shape the transcription of specific genes and, therefore, cellular functions. This review will explore the emerging evidence for the role of epigenetic modifications in programming the legacy of hyperglycaemia for kidney disease in diabetes.