Genetics of macrovascular complications in type 2 diabetes

Abstract

Type 2 diabetes mellitus (T2DM) is a metabolic disorder that currently affects more than 400 million worldwide and is projected to cause 552 million cases by the year 2030. Long-term vascular complications, such as coronary artery disease, myocardial infarction, stroke, are the leading causes of morbidity and mortality among diabetic patients. The recent advances in genome-wide technologies have given a powerful impetus to the study of risk markers for multifactorial diseases. To date, the role of genetic and epigenetic factors in modulating susceptibility to T2DM and its vascular complications is being successfully studied that provides the accumulation of genomic knowledge. In the future, this will provide an opportunity to reveal the pathogenetic pathways in the development of the disease and allow to predict the macrovascular complications in T2DM patients. This review is focused on the evidence of the role of genetic variants and epigenetic changes in the development of macrovascular pathology in diabetic patients.

Study on the active ingredients and mechanism of action of Jiaotai Pill in the treatment of type 2 diabetes based on network pharmacology: A review

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Vascular complications of diabetes: A narrative review

“…[ 85 ] In addition, recent genome-wide studies have unveiled genetic variation and epigenetic alterations as risk factors for CAD complications in patients with diabetes. [ 86 ] Jeanette Erdmann et al summarized 163 CAD risk loci based on 10 years of genome-wide association studies. [ 65 ] These loci may be useful for improved prediction of CAD risk and for encouraging preventive measures.…”

Micro-ribonucleic acid modulation with oxidative stress and inflammation in patients with type 2 diabetes mellitus – a review article

“…Impaired insulin signaling, oxidative stress, and inflammation initiate endothelial dysfunction and rapidly promote atherosclerosis development in T2D patients [ 91 ]. Many miRNAs have important roles in the regulation of the immune system, inflammatory response, and platelet function, which are the key factors not only in atherosclerosis development but also in the clinical manifestation of the disease [ 92 ].…”