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necrotic tissue and matrix debris from the damaged myocardium ( Frangogiannis 2012 , Yan et al . 2013 ), but they are also important to ensure transition to repair. Macrophage polarization toward a reparative phenotype in the healing myocardium is
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( Friedman & Halaas 1998 ). Leptin stimulates monocytes and macrophages to produce proinflammatory cytokines including: IL6, TNFa and IL12 ( Gainsford et al . 1996 ) and stimulates CCL2 production in human hepatic stellate cells ( Aleffi et al . 2005
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characterized by excessive deposition of ECM, fibrotic diseases are also accompanied by an inflammatory response involving monocyte/macrophage activation, and thus attempts to control the progress of these diseases with anti-inflammatory therapies have been
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metabolic syndrome ( Hotamisligil et al . 1993 , 1995 ). The crosstalk between adipocytes and macrophages which infiltrate adipose tissue in obesity is considered to be crucial for the development of the pro-inflammatory state ( Bluher 2008 ). To date, the
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macrophages and neutrophils are part of the innate immune system and serve as the first line of defense for eliminating pathogens ( Lingen 2001 ). They set up inflammatory signaling programs in response to an infection and eliminate pathogens through
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pro-inflammatory cell types, most notably macrophages ( Lumeng et al. 2007 ). Macrophage infiltration has also been demonstrated by a number of groups ( Hevener et al. 2007 , Fink et al. 2014 ), but not all ( Tam et al. 2012 ), to be a feature
Department of Medicine, Monash University, Clayton, Victoria, Australia
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, to be operative in vascular beds ( McCurley et al. 2012 ) and discrete subpopulations of hypothalamic neurones ( Gasparini et al. 2019 ), whereas the MR, in monocyte/macrophages, cardiomyocytes, adipocytes and hippocampal neurones, is unprotected
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catecholamine turnover of in the iWAT, and the issue catecholamine levels were not affected (WT 18.8 vs H4-TG 16.2 pg/µg protein). The contribution of macrophage to catecholamine secretion is under debate ( Qiu et al. 2014 , Fischer et al. 2017 , Reitman
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Institute of Health Research-INCLIVA, Endocrinology and Nutrition Department Clinic Hospital and Department of Medicine, CIBER de Diabetes y Enfermedades Metabólicas asociadas (CIBERDEM), Department of Farmacology, Centro de Investigación Príncipe Felipe, Avenida Menéndez Pelayo, 4, 46010 Valencia, Spain
Institute of Health Research-INCLIVA, Endocrinology and Nutrition Department Clinic Hospital and Department of Medicine, CIBER de Diabetes y Enfermedades Metabólicas asociadas (CIBERDEM), Department of Farmacology, Centro de Investigación Príncipe Felipe, Avenida Menéndez Pelayo, 4, 46010 Valencia, Spain
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Institute of Health Research-INCLIVA, Endocrinology and Nutrition Department Clinic Hospital and Department of Medicine, CIBER de Diabetes y Enfermedades Metabólicas asociadas (CIBERDEM), Department of Farmacology, Centro de Investigación Príncipe Felipe, Avenida Menéndez Pelayo, 4, 46010 Valencia, Spain
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Institute of Health Research-INCLIVA, Endocrinology and Nutrition Department Clinic Hospital and Department of Medicine, CIBER de Diabetes y Enfermedades Metabólicas asociadas (CIBERDEM), Department of Farmacology, Centro de Investigación Príncipe Felipe, Avenida Menéndez Pelayo, 4, 46010 Valencia, Spain
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Institute of Health Research-INCLIVA, Endocrinology and Nutrition Department Clinic Hospital and Department of Medicine, CIBER de Diabetes y Enfermedades Metabólicas asociadas (CIBERDEM), Department of Farmacology, Centro de Investigación Príncipe Felipe, Avenida Menéndez Pelayo, 4, 46010 Valencia, Spain
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section analysis of both groups of mice ( Fig. 3 A images). Immunohistochemical analysis of the F4/80 macrophage marker also showed increased (kuppfer) macrophage infiltration in the liver of HL −/− mice compared with that in WT mice ( Fig. 3 B, P <0
Biomedical Research Group, UCD School of Biomolecular and Biomedical Sciences, School of Biomedical Sciences, School of Physical Education, Department of Science, Institute of Technology Tallaght, Dublin, Ireland
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-lymphocytes and macrophages, leading to microenvironmental changes, resulting in β-cell injury and death ( Masters et al . 2010 ). Destruction of β-cells during islet inflammation can be mediated by direct contact with activated macrophages and by exposure to