Key result
Current therapeutic options and potential future treatment approaches for inflammatory cardiomyopathy are reviewed based on mechanistic insights from the experimental autoimmune myocarditis mouse model.
Mechanistic insights from the experimental autoimmune myocarditis mouse model may inform future therapeutic strategies for inflammatory cardiomyopathy.
Should not change clinical practice for inflammatory cardiomyopathy; hypothesis-generating insights from mouse models warrant translational research.
Inflammatory cardiomyopathy is a common cause of heart failure developing on a basis of cardiac inflammation. Cardiac inflammation - or myocarditis - is usually triggered by infections or cardiac damage of any cause. Experimental autoimmune myocarditis refers to a CD4(+) T cell-mediated mouse model of inflammatory cardiomyopathy. So far, the experimental autoimmune myocarditis model helped us to understand the role of various chemokines, cytokines, and cell subsets in the progression of inflammatory heart disease. Here, we review the current therapeutic options for inflammatory cardiomyopathy, and delineate potential future treatment approaches from the most recent mechanistic insights given by the experimental autoimmune myocarditis model.
No takes yet. Share an insight, caveat, or question.
Błyszczuk et al. (2008) conducted a review in Inflammatory cardiomyopathy. Current therapeutic options and potential future treatment approaches for inflammatory cardiomyopathy are reviewed based on mechanistic insights from the experimental autoimmune myocarditis mouse model.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: