naa a22 4500 510787576 CHVBK 20180411083307.0 cr unu---uuuuu 180411e20131201xx s 000 0 eng 10.1007/s12041-013-0288-1 doi (NATIONALLICENCE)springer-10.1007/s12041-013-0288-1 Human genetics of diabetic vascular complications [Elektronische Daten] [ZI-HUI TANG, ZHOU FANG, LINUO ZHOU] Diabetic vascular complications (DVC) affecting several important organ systems of human body such as the cardiovascular system constitute a major public health problem. There is evidence demonstrating that genetic factors contribute to the risk of DVC genetic variants, structural variants, and epigenetic changes play important roles in the development of DVC. Genetic linkage studies have uncovered a number of genetic loci that may shape the risk of DVC. Genetic association studies have identified many common genetic variants for susceptibility to DVC. Structural variants such as copy number variation and interactions of gene × environment have also been detected by association analysis. Apart from the nuclear genome, mitochondrial DNA plays a critical role in regulation of development of DVC. Epigenetic studies have indicated epigenetic changes in chromatin affecting gene transcription in response to environmental stimuli, which provided a large body of evidence of regulating development of diabetes mellitus. Recently, a new window has opened on identifying rare and common genetic loci through next generation sequencing technologies. This review focusses on the current knowledge of the genetic and epigenetic basis of DVC. Ultimately, identification of genes or genetic loci, structural variants and epigenetic changes contributing to risk of or protection from DVC will help uncover the complex mechanism(s) underlying DVC, with crucial implications for the development of personalized medicine for diabetes mellitus and its complications. Indian Academy of Sciences, 2013 diabetic vascular complications nationallicence genetics nationallicence epigenetic nationallicence mitochondrial DNA nationallicence interactions of gene × environment nationallicence TANG ZI-HUI Department of Endocrinology and Metabolism, Fudan University Huashan Hospital, 200040, Shanghai, People's Republic of China aut FANG ZHOU Department of Endocrinology and Metabolism, Fudan University Huashan Hospital, 200040, Shanghai, People's Republic of China aut ZHOU LINUO Department of Endocrinology and Metabolism, Fudan University Huashan Hospital, 200040, Shanghai, People's Republic of China aut Journal of Genetics Springer India 92/3(2013-12-01), 677-694 0022-1333 92:3<677 2013 92 12041 https://doi.org/10.1007/s12041-013-0288-1 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s12041-013-0288-1 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- TANG ZI-HUI Department of Endocrinology and Metabolism, Fudan University Huashan Hospital, 200040, Shanghai, People's Republic of China aut NATIONALLICENCE 700 1- FANG ZHOU Department of Endocrinology and Metabolism, Fudan University Huashan Hospital, 200040, Shanghai, People's Republic of China aut NATIONALLICENCE 700 1- ZHOU LINUO Department of Endocrinology and Metabolism, Fudan University Huashan Hospital, 200040, Shanghai, People's Republic of China aut NATIONALLICENCE 773 0- Journal of Genetics Springer India 92/3(2013-12-01), 677-694 0022-1333 92:3<677 2013 92 12041 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer