CCR2 modulates inflammatory and metabolic effects of high-fat feeding.

By S. Weisberg, Deborah Hunter, R. Huber, Jacob Lemieux, S. Slaymaker, K. Vaddi, I. Charo, Rudolph L. Leibel, A. Ferrante. Journal of Clinical Investigation, 2006

1,613 citations recorded by the source corpus.

Subfields: Epidemiology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/77a5fdbf92aee110ee0af6dd277fa96391c58b60

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Citations in the corpus

Macrophage plasticity and polarization: in vivo veritas. (2012, neutral): “(101, 103, 104) and by the macrophage-derived apoptosis inhibitor of macrophages (AIM) (105).”
Phenotypic Switching of Adipose Tissue Macrophages With Obesity Is Generated by Spatiotemporal Differences in Macrophage Subtypes (2008, background): “Blockade of CCR2 has been proposed as one way to accomplish this (2).”
Adipokines in inflammation and metabolic disease (2011, background): “Studies of mice with a somatic deletion of CC-chemokine receptor 2 ( Ccr2 ), the receptor for CCL2, gain as much weight as their wild-type littermates but fail to show adipose tissue inflammation, and maintain insulin sensitivity on a high-fat die”
Adipose tissue as an endocrine organ. (2010, background): “Adipocyte-derived factors, such as MCP-1 or CSFare overexpressed in obesity and can promote the recruitment of irculating monocytes (Weisberg et al., 2006).”
Increased Inflammatory Properties of Adipose Tissue Macrophages Recruited During Diet-Induced Obesity (2007, background): “Recruited ATMs had increased expression of Ccr2, Il6, and Nos2, genes that have been previously shown to contribute to inflammation in adipose tissue (5,6,12).”
Adipose tissue plasticity in health and disease (2022, background): “Similarly, reducing macrophage recruitment into adipose tissue ameliorates metabolic complications in high-fat-fed mice (Kanda et al., 2006; Weisberg et al., 2006).”
The cellular and signaling networks linking the immune system and metabolism in disease (2012, background): “Deletion of macrophage CCR2 or adipose-tissue MCP-1 can lead to a decrease in ATM content in obesity, reduce tissue markers of inflammation and ameliorate insulin resistanc”
Macrophage-mediated inflammation in metabolic disease (2011, background): “First, mice lacking CC-chemokine receptor 2 (CCR2), which is required for the trafficking of inflammatory monocytes and macrophages into tissues, are protected from obesity-induced inflammation and insulin resistanc”
Intestinal mucosal adherence and translocation of commensal bacteria at the early onset of type 2 diabetes: molecular mechanisms and probiotic treatment (2011, positive): “In addition, we showed that antibiotics and dietary ﬁbres, most likely acting by changing the intestinal microbiota of HFD-fed mice, can reduce metabolic endotoxemia, inﬂammation, and improve the overall impaired metabolism (Cani et al, 2007b, 2008; Membrez et al, 2008).”
Adipose Tissue in Obesity-Related Inflammation and Insulin Resistance: Cells, Cytokines, and Chemokines (2013, positive): “Overexpression, deficiency, or mutation-induced dysfunction of MCP-1 in differentmousemodelswere shown to interferewithATMs accumulation, along with insulin-resistance development [95, 96].”