High glucose induces DNA methyltransferase 1 dependent epigenetic reprogramming of the endothelial exosome proteome in type 2 diabetes.

In response to hyperglycemia, endothelial cells (ECs) release exosomes with altered protein content and contribute to paracrine signalling, subsequently leading to vascular dysfunction in type 2 diabetes (T2D). High glucose reprograms DNA methylation patterns in various cell/tissue types, including ECs, resulting in pathologically relevant changes in cellular and extracellular proteome. However, DNA methylation-based proteome reprogramming in endothelial exosomes and associated pathological implications in T2D are not known.

Neutrophil sub-types in maintaining immune homeostasis during steady state, infections and sterile inflammation.

Introduction: Neutrophils are component of innate immune system and a) eliminate pathogens b) maintain immune homeostasis by regulating other immune cells and c) contribute to the resolution of inflammation. Neutrophil mediated inflammation has been described in pathogenesis of various diseases. This indicates neutrophils do not represent homogeneous population but perform multiple functions through confined subsets.

Ethnic disparities attributed to the manifestation in and response to type 2 diabetes: insights from metabolomics.

Type 2 diabetes (T2D) associated health disparities among different ethnicities have long been known. Ethnic variations also exist in T2D related comorbidities including insulin resistance, vascular complications and drug response. Genetic heterogeneity, dietary patterns, nutrient metabolism and gut microbiome composition attribute to ethnic disparities in both manifestation and progression of T2D.