The damaging nature of extracellular RNA in cardiovascular diseases
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Abstract
After vessel damage or injury, atherosclerosis and vascular remodeling are driven by inflammation and mononuclear cell infiltration. Macrophages respond to external stimuli with rapid changes in their expression of many inflammation-related genes to undergo polarization towards the M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotype. This unique property of macrophages allows these cells to modulate chronic inflammatory processes such as atherogenesis. Cardiomyocyte death occurs during acute myocardial infarction under situations of cardiac ischemia/reperfusion resulting in a major impact on the quality of life and survival of patients suffering from coronary artery disease. Despite optimal therapy, the morbidity and mortality of patients presenting with an acute myocardial infarction (MI) remain significant. Self-extracellular RNA (eRNA) has recently been implicated by our group to become enriched at sites of tissue damage, and to act as a proinflammatory mediator. In thus study, the role of eRNA in high-fat-diet (HFD)-induced atherosclerosis in mice was documented. Given the association of eRNA with macrophages within atherosclerotic lesions, it was assessed whether eRNA generated by the macrophages themselves may induce inflammatory responses within these cells, independent of Toll-like receptor signaling. Moreover, the role of eRNA as a novel therapeutic target for protecting the heart against the detrimental effect of acute ischemia/reperfusion (I/R) injury was observed.Link to publications or other datasets
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Giessen : VVB Laufersweiler