Macrophage myeloperoxidase regulation by granulocyte macrophage colony-stimulating factor in human atherosclerosis and implications in acute coronary syndromes.

By S. Sugiyama, Y. Okada, G. Sukhova, Renu Virmani, J. Heinecke, Peter Libby. American Journal of Pathology, 2001

721 citations recorded by the source corpus.

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Citations in the corpus

Association between myeloperoxidase levels and risk of coronary artery disease. (2001, background): “Macrophages containing MPO and MPO-dependent oxidation products are selectively enriched in atheromas that have undergone plaque rupture and ulceration.(22) Moreover, hypochlorous acid (HOCl), a primary oxidant generated by MPO,(38) may promote extracellular matrix degradation in vivo.”
Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target? (2019, background): “Macrophages play critical roles in atherogenesis through their pro-inflammatory properties that assist in the destabilization of atheroma by degrading ECM and hence promoting erosion or rupture of plaques, which ultimately culminates in occlusive thrombus formation [49].”
Reactive Oxygen Species in Cardiovascular Disease (2011, background): “Macrophages in eroded or ruptured plaques are rich in MPO compared to macrophages in fatty streaks that contain little MPO [181].”
A Myeloperoxidase-Containing Complex Regulates Neutrophil Elastase Release and Actin Dynamics during NETosis (2014, neutral): “Inﬂammatory monocytes express MPO and are implicated in cardiovascular disease (Sugiyama et al., 2001).”
Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease. (2004, background): “MPO (28, 29), and multiple specific oxidation products formed by the enzyme (8, 16, 30, 31), are markedly enriched within human atherosclerotic lesions.”
Pathology of the vulnerable plaque. (2007, background): “In addition to providing a pro-oxidant ilieu and increasing oxidized low-density lipoprotein choleserol, there is evidence that macrophage MPO might be esponsible for the disruption of the fibrous cap by production ypochlorous acid (8).”
Myeloperoxidase: friend and foe (2005, background): “However, the reinstitution of MPO synthesis in mature macrophages in atherosclerotic lesions, possibly under the control of granulocyte macrophage-colony stimulating factor [461], is an intriguing possibility.”
Inflammation in atherosclerosis (2002, background): “GM-CSF aids the survival of a population of mononuclear phagocytes that contain myeloperoxidase, an enzyme that gives rise to the pro-oxidant hypochlorous acid, a potential source of oxidative stress and inflammation in the human plaqu”