Clinically, the inflammation and oxidative stress of perirenal adipose tissue (PAT) may have close relation with the development of cardiovascular diseases, especially systemic hypertension.
A growing body of evidence supports a facilitatory role for EAT inflammation in cardiovascular disease.
EAT is also a source of multipotent stem or progenitor-like cell populations, which are deemed to be involved in the tissue repair and in the pathogenesis of cardiovascular disease. EAT is an unusual visceral fat depot with anatomical and functional contiguity to the myocardium and coronary arteries that may serve a unique role and thus may differ from other visceral fat tissues depots. Recent studies have called attention to a role for epicardial adipose tissue (EAT) inflammation as an additional determinant of inflammation and susceptibility to cardiovascular disease in patients with obesity and metabolic syndrome. White adipose tissue is highly adapted to store excess energy as triglycerides, while brown adipose tissue functions to dissipate chemical energy in the form of heat. Additionally, we have demonstrated a downregulation of brown adipose tissue specific genes such as uncoupling protein ( Ucp) -1 and an upregulation of genes specific to white adipose tissue by air pollution exposure. A characteristic hallmark in these studies was the development of adipose inflammation in visceral fat tissues characterized by the infiltration of innate immune cells and pro-inflammatory gene expression. We and others have described recent findings that have linked air-pollution exposure in animal models to the development of insulin resistance and inflammation. The inflammation in adipose depots has been widely linked to systemic abnormalities including disturbances in glucose homeostasis, lipid abnormalities and accelerated development of cardiovascular disease. The term “metaflammation” is widely used to describe the close dependence of metabolic abnormalities to inflammation in the visceral fat tissues. Adipose inflammation is a characteristic hallmark of Type II diabetes-obesity states characterized by insulin resistance.
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