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Updated: Mar 14, 2026
Isolation of Adipose Tissue Immune Cells
Published on: May 22, 2013
Blocking CXCR7-mediated adipose tissue macrophages chemotaxis attenuates insulin resistance and inflammation in
Hongxia Peng1, Hu Zhang1, Honglei Zhu2
1Department of Endocrinology, Shangqiu First People's Hospital, Shangqiu 476100, China.
Abstract:
Adipose tissue macrophages (ATMs) have been considered to have a pivotal role in the chronic inflammation development during obesity. Although chemokine-chemokine receptor interaction has been studied in ATMs infiltration, most chemokine receptors remain incompletely understood and little is known about their mechanism of actions that lead to ATMs chemotaxis and pathogenesis of insulin resistance during obesity. In this study, we reported that CXCR7 expression is upregulated in adipose tissue, and specifically in ATMs during obesity. In addition, CXCL11 or CXCL12-induced ATMs chemotaxis is mediated by CXCR7 in obesity but not leanness, whereas CXCR3 and CXCR4 are not involved. Additional mechanism study shows that NF-κB activation is essential in ATMs chemotaxis, and manipulates chemotaxis of ATMs via CXCR7 expression regulation in obesity. Most importantly, CXCR7 neutralizing therapy dose dependently leads to less infiltration of macrophages into adipose tissue and thus reduces inflammation and improves insulin sensitivity in obesity. In conclusion, these findings demonstrated that blocking CXCR7-mediated ATMs chemotaxis ameliorates insulin resistance and inflammation in obesity.
Insights
Blocking CXCR7, a receptor on adipose tissue macrophages, reduces inflammation and improves insulin sensitivity in obesity. This targeted therapy lessens macrophage infiltration, offering a new approach to managing obesity-related metabolic dysfunction.
Area of Science:
- Immunology
- Metabolic Diseases
- Molecular Biology
Background:
- Adipose tissue macrophages (ATMs) play a key role in obesity-related chronic inflammation.
- The specific mechanisms of ATM chemotaxis and their contribution to insulin resistance are not fully understood.
- Chemokine receptor involvement in ATM infiltration during obesity requires further elucidation.
Purpose of the Study:
- To investigate the role of CXCR7 in ATM chemotaxis and insulin resistance during obesity.
- To elucidate the signaling pathways regulating ATM migration in obese adipose tissue.
- To evaluate the therapeutic potential of targeting CXCR7 in obesity.
Main Methods:
- Quantification of CXCR7 expression in adipose tissue and ATMs from obese and lean subjects.
- Assessment of ATM chemotaxis induced by CXCL11/CXCL12, with investigation of CXCR3, CXCR4, and CXCR7 involvement.
- Analysis of NF-κB activation and its role in CXCR7-mediated ATM chemotaxis.
- Administration of CXCR7 neutralizing therapy in an obesity model and evaluation of its effects on macrophage infiltration, inflammation, and insulin sensitivity.
Main Results:
- CXCR7 expression is significantly upregulated in adipose tissue and ATMs during obesity.
- CXCR7 mediates CXCL11/CXCL12-induced ATM chemotaxis in obesity, independent of CXCR3 and CXCR4.
- NF-κB activation is crucial for ATM chemotaxis and regulates CXCR7 expression in obesity.
- CXCR7 neutralizing therapy dose-dependently reduced macrophage infiltration, decreased inflammation, and improved insulin sensitivity in obese subjects.
Conclusions:
- CXCR7 is a key mediator of ATM chemotaxis in obesity.
- Targeting CXCR7-mediated ATM migration offers a promising therapeutic strategy for ameliorating obesity-induced inflammation and insulin resistance.
