Key result
Dysfunctional perivascular adipose tissue (PVAT) observed in metabolic syndrome loses its thermogenic phenotype through 'PVAT whitening', which is influenced by epigenetic factors and contributes to cardiometabolic diseases.
This review highlights the role of epigenetic regulation in perivascular adipose tissue dysfunction and its contribution to cardiometabolic diseases like atherosclerosis.
Hypothesis-generating for epigenetic targeting of PVAT; prospective trials needed before clinical consideration.
Perivascular adipose tissue (PVAT) has emerged in the past decades as an integral part of the vasculature (tunica adiposa), contributing by the release of adipokines, to important physiological process such as vascular tone regulation. The metabolic syndrome is associated with an increase deposition of PVAT and the development of atherosclerosis. Whereas healthy PVAT protect the vasculature from inflammation, lipid accumulation and hypothermia, the dysfunctional PVAT observed in the metabolic syndrome favour many features of atherosclerosis such as endothelial dysfunction, vascular smooth muscle proliferation and inflammation. The down- and up-regulation of adiponectin, leptin and nerve growth factor, respectively in the dysfunctional PVAT perfectly illustrates this change. Phenotypically, healthy PVAT resembles the thermogenic brown and beige adipocytes, however, recent data suggest a loss of PVAT thermogenic phenotype during the metabolic syndrome in a process called `PVAT whitening`. This review will provide a current perspective on the factors susceptible to influence PVAT epigenetics and the consequences of PVAT dysfunction on cardiometabolic diseases.
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Karl Blirando (2017) conducted a review in Cardiometabolic diseases. Epigenetic regulation of perivascular adipose tissue was evaluated. Dysfunctional perivascular adipose tissue (PVAT) observed in metabolic syndrome loses its thermogenic phenotype through 'PVAT whitening', which is influenced by epigenetic factors and contributes to cardiometabolic diseases.
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