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Circulating ANGPTL2 levels increase in mice with heart failure. Increased circulating ANGPTL2 levels in mice reflect, rather than promote, cardiac dysfunction.
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The ANGPTL2 played an essential role in osteoclast generation through regulating the proliferation and inflammation of osteoclast lineage cells, providing new insights into the therapeutic strategy to alleviate bone loss.
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ANGPTL2 up-regulation in skeletal myocytes accelerates muscle atrophy, and exercise-induced attenuation of ANGPTL2 expression in those tissues may partially explain how exercise training prevents sarcopenia.
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Angptl2(-/-) in paraquat-treated mice attenuated acute lung injury progression by reducing the number of total cells, total leukocytes, neutrophils and macrophages in bronchoalveolar lavage fluid and reducing inflammatory response through the inactivation of nuclear factor kappa B pathway.
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Kaempferol modulates the expression of ANGPTL2 to lessen the mastitis in mice.
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These results support the importance of ANGPTL2 in the stem cell niche in regulating stemness and epithelial wound healing in the intestine.
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we provide the first evidence for ANGPTL2 function in the acute ischemic brain. Infiltrated macrophage-derived ANGPTL2 enhanced inflammatory responses and was associated with severe brain tissue damage in the acute phase of ischemic stroke.
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Angptl2 deficiency in lung epithelial cells and resident alveolar macrophages causes severe lung fibrosis seen following bleomycin treatment, suggesting that ANGPTL2 derived from these cell types plays a protective role against fibrosis in lung.
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Angptl2 regulates not only adipose tissue metabolism but also bone metabolism
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findings suggest that macrophage-derived ANGPTL2 promotes an innate immune response in those cells by enhancing proinflammatory activity and NO production required to fight infection.
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Angptl2 might therefore represent a multistep regulator of CNV pathogenesis and serve as a new therapeutic target for age-related macular degeneration.
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ANGPTL2 promotes adipose tissue macrophage and T lymphocyte accumulation and leads to insulin resistance.
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It plays a role in tumor progression.
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Angptl2 induces proinflammatory responses in peritoneal macrophages and monocytes.
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In angptl2 knockdown mice, ACh-mediated endothelium-dependent vasodilation was greater than in WT mice. Lack of angptl2 expression limits the metabolic stress induced by a high-fat diet and maintains endothelial function in mice.
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knockdown of angptl2 may be protective against ANG II-induced cerebral endothelial dysfunction; it favors the production of NO increasing endothelial cell resistance to stress.
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Angptl2 expression was reduced in PHD3(-/-) bone-marrow-derived macrophages under stress conditions. PHD3 affects the production of Angptl2 and additionally influences the response toward this apoptosis-modulating factor.
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Angptl2-induced inflammation increases susceptibility to microenvironmental changes, allowing increased oxidative stress and decreased Msh2 expression.
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Endothelial cell-derived Angptl2 accelerates vascular inflammation by activating proinflammatory signaling in endothelial cells and increasing macrophage infiltration, leading to endothelial dysfunction and atherosclerosis progression.
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periodic expression of ANGPTL2 is regulated by a molecular clock