Lack of macrophage fatty-acid–binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis

By L. Makowski, Jeffrey B. Boord, K. Maeda, V. Babaev, K. Uysal, Maureen A. Morgan, R. Parker, J. Suttles, S. Fazio, G. Hotamışlıgil and 1 more. Nature Medicine, 2001

686 citations recorded by the source corpus.

Subfields: Cancer Research, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7a456adc8bdd5828919efc561ff81e661eee1fcf

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In Cancer Research

G. Hotamışlıgil

In Epidemiology

In Molecular Biology

Citations in the corpus

Obesity is associated with macrophage accumulation in adipose tissue. (2003, background): “However, macrophages and adipocytes express a number of genes in common, including Cd36 (50), Pparg (51), and aP2 (52).”
MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. (2006, background): “However, given that 3 types of transgene controlled by the aP2 gene promoter were shown to be expressed in macrophages of mice (27), we cannot exclude the possibility that the MCP-1 transgene was expressed in macrophages of our MCP-1 Tg-B mice and that the MCP-1 produced by these cells contributed t”
Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, positive): “As the lipotoxicity of immune cells such as macrophages is a common feature of obesity and atherosclerosis, the action of lipid chaperones in controlling lipid-induced ER stress has critical implications for these diseases and their complications (Erbay et al., 2009; Makowski et al., 2001).”
CARNITINE TRANSPORT AND FATTY ACID OXIDATION (2016, neutral): “There are no reported human phenotypes and knock-out mice show inconsistent or no phenotypes [50-60].”
Transcriptional control of adipose lipid handling by IRF4 (2011, neutral): “This is problematic because Fabp4 is expressed in macrophages as well as in fat (Fu et al., 2002; Makowski et al., 2001).”
Obesity-induced inflammatory changes in adipose tissue. (2003, background): “” Chronic hyperglycemia has been shown to induce multiple defects in β cells, including early decreases in glucose-stimulated insulin secretion, and late irreversible changes in insulin-gene transcription and β cell mass (7, 8).”
Inflammation and insulin resistance. (2003, background): “Mice lacking aP2 are less able to produce cholesterol esters and, thus, to form foam cells (15).”
Adipocytokines in Obesity and Metabolic Disease (2014, neutral): “Despite long having been considered an adipocyte-specific protein, aP2 was found to be expressed in the macrophages (Makowski et al. 2001) and can be quickly induced by endotoxin (Kazemi et al.”
Recent advances in the relationship between obesity, inflammation, and insulin resistance. (2006, background): “Moreover, numerous genes that code for transcription factors, cytokines, inflammatory signalling molecules, and fatty acid transporters are essential for adipocyte biology, and are also expressed and functional in macrophages [17-19].”
Inflammation, stress, and diabetes. (2005, positive): “Animals lacking the adipocyte/macrophage FABPs ap2 and mal1 are strongly protected against type 2 diabetes and atherosclerosis, a phenotype reminiscent of that of thiazolidinedi-one-treated (TZD-treated) mice and humans (27, 84, 85).”