Abstract
Obesity is characterized as a complex and multifactorial excess accretion of adipose tissue accompanied with alterations in the immune and metabolic responses. Although the chemokine systems have been documented to be involved in the control of tissue inflammation and metabolism, the dual role of chemokines and chemokine receptors in the pathogenesis of the inflammatory milieu and dysregulated energy metabolism in obesity remains elusive. The objective of this review is to present an update on the link between chemokines and obesity-related inflammation and metabolism dysregulation under the light of recent knowledge, which may present important therapeutic targets that could control obesity-associated immune and metabolic disorders and chronic complications in the near future. In addition, the cellular and molecular mechanisms of chemokines and chemokine receptors including the potential effect of post-translational modification of chemokines in the regulation of inflammation and energy metabolism will be discussed in this review.
Highlights
Sci. 2021, 22, 13528. https://doi.org/The chemokines and seven-transmembrane G protein-coupled chemokine receptors have been documented to be the mediators of immune cell migration and response to the inflammatory reaction in injury and infection
This review aims to present a significant updated study about the physiological and pathological roles of chemokines in energy metabolism and inflammation in the states of normal weight and obesity and the possible underlying mechanisms
Increased adipose tissue expression of CCL19 in obese subjects has been implicated to represent a pathological link between systemic low-grade inflammation and insulin resistance [19]. These observations demonstrate that the chemokines/chemokine receptor-mediated signaling substantially contribute to the development of adipose tissue inflammation and subsequent metabolic disorders in obesity
Summary
The chemokines and seven-transmembrane G protein-coupled chemokine receptors have been documented to be the mediators of immune cell migration and response to the inflammatory reaction in injury and infection. Chemokines have been reported to coordinate recruitment of various cell types in adipose tissues such as immune cells, adipocyte progenitors and endothelial cells in mice and humans [1]. The interaction between the chemokine system and these different cell types in brown and white adipose tissues (WAT). The dynamic interaction between chemokines and different subsets of mesenchymal cells in the pathogenesis of the inflammatory milieu and dysregulated energy metabolism in obesity remains poorly understood. This review aims to present a significant updated study about the physiological and pathological roles of chemokines in energy metabolism and inflammation in the states of normal weight and obesity and the possible underlying mechanisms.
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