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Leslie T. Cooper, DeLisa Fairweather, Nano-scale treatment for a macro-scale disease: nanoparticle-delivered siRNA silences CCR2 and treats myocarditis, European Heart Journal, Volume 36, Issue 23, 14 June 2015, Pages 1434–1436, https://doi.org/10.1093/eurheartj/ehu302
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This editorial refers to ‘Silencing of CCR2 in myocarditis’†, by F. Leuschner et al., on page 1478.
Myocarditis is a significant cause of sudden death, acute heart failure, and chronic dilated cardiomyopathy.1 The cellular and molecular pathogenesis of chronic dilated cardiomyopathy that sometimes follows acute myocarditis has been explored in animal models but is not well understood in human disease. Clinical myocarditis research has largely focused on modifying the mediators of acute myocarditis based on the theory that lowering acute inflammation may prevent long-term left ventricular remodelling. However, the primary mediators of fibrosis and chronic cardiomyopathy can differ from those involved in the acute immunological reaction that initially leads to cardiac inflammation.
Although T cells are important in the pathogenesis of acute myocarditis, CD11b+ monocytes/macrophages are the most common cardiac inflammatory cell in myocarditis patients and in viral and experimental autoimmune myocarditis (EAM) mouse models.2–6 Strategies aimed at blocking CD11b+ cells and the profibrotic pathways they can mediate may impact the long-term cardiac damage from myocarditis. One attractive target is the receptor for monocyte chemotactic protein 1 (MCP-1), also named chemokine (C-C motif) ligand 2 (CCL2).7
