The pathophysiology of obesity is complex and includes changes in eating behavior, genetic, epigenetic, environmental factors, and much more. To date, ~40 genetic polymorphisms are associated with obesity and fat distribution. However, since these options do not fully explain the inheritance of obesity, other options, such as epigenetic changes, need to be considered. Epigenetic modifications affect gene expression without changing the deoxyribonucleic acid sequence. In addition, environmental exposure during critical periods of development can affect the epigenetic tags and lead to obesity. A deeper understanding of the epigenetic mechanisms underlying obesity can aid in prevention based on lifestyle changes. This review focuses on the role of epigenetic modifications in the development of obesity and related conditions.

Perivascular adipose tissue (PVAT) is an active regulator of vascular homeostasis. In physiological conditions, it maintains normal function of vessels, releasing antiatherogenic, anti-inflammatory and vasodilating biologically active substances. Dysfunctional PVAT secretes pro-inflammatory cytokines and adipokines, which play an important role in the development of cardiovascular diseases. This review considers the PVAT function in health and disease, its contribution to the pathogenesis of atherosclerosis, hypertension, aortic aneurysm and vasculitis. In addition, novel methods of non-invasive PVAT assessment and potential strategies for targeted treatment of cardiovascular diseases are presented.