Abstract
Adipose tissue is a critical regulator of systemic metabolism and bodily homeostasis as it secretes a myriad of adipokines, including inflammatory and anti-inflammatory cytokines. As the main storage pool of lipids, subcutaneous and visceral adipose tissues undergo marked hypertrophy and hyperplasia in response to nutritional excess leading to hypoxia, adipokine dysregulation, and subsequent low-grade inflammation that is characterized by increased infiltration and activation of innate and adaptive immune cells. The specific localization, physiology, susceptibility to inflammation and the heterogeneity of the inflammatory cell population of each adipose depot are unique and thus dictate the possible complications of adipose tissue chronic inflammation. Several lines of evidence link visceral and particularly perivascular, pericardial, and perirenal adipose tissue inflammation to the development of metabolic syndrome, insulin resistance, type 2 diabetes and cardiovascular diseases. In addition to the implication of the immune system in the regulation of adipose tissue function, adipose tissue immune components are pivotal in detrimental or otherwise favorable adipose tissue remodeling and thermogenesis. Adipose tissue resident and infiltrating immune cells undergo metabolic and morphological adaptation based on the systemic energy status and thus a better comprehension of the metabolic regulation of immune cells in adipose tissues is pivotal to address complications of chronic adipose tissue inflammation. In this review, we discuss the role of adipose innate and adaptive immune cells across various physiological and pathophysiological states that pertain to the development or progression of cardiovascular diseases associated with metabolic disorders. Understanding such mechanisms allows for the exploitation of the adipose tissue-immune system crosstalk, exploring how the adipose immune system might be targeted as a strategy to treat cardiovascular derangements associated with metabolic dysfunctions.
Highlights
Over the past two decades, the traditional view of adipose tissue (AT) as a passive store of excess calories evolved to implicate an endocrine role that is pertinent to glucose and lipid homeostasis [1]
We have shown that PVAT localized inflammation, which was associated with uncoupling protein 1 (UCP1)-mediated hypoxic preconditioning, occurs in isolation of systemic inflammation in a prediabetic rat model [32]
We recently identified an increased expression of UCP1 in PVAT of HFD-fed rats, which was associated with localized PVAT inflammation contributing to metabolic syndrome (MetS)-associated vascular dysfunction [32]
Summary
Over the past two decades, the traditional view of adipose tissue (AT) as a passive store of excess calories evolved to implicate an endocrine role that is pertinent to glucose and lipid homeostasis [1]. AT-resident eosinophils produce IL-4 and IL-13 that drive macrophage M2 polarization, trigger Th2 differentiation, enhance B cell activation and promote metabolic homeostasis [209, 210]. MCs are enriched in visceral AT of mice and humans and are increased in settings of obesity and T2D, where they drive AT inflammation partly by enhancing macrophage infiltration [21, 221, 222].
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