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Myosin-specific CD4+ T cells drive progressive inflammatory cardiomyopathy in TCRM mice, while global longitudinal strain at 6 weeks predicts disease progression.
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This editorial highlights the translational value of the TCRM mouse model in demonstrating that myosin-specific CD4+ T cells drive inflammatory cardiomyopathy and that early echocardiographic global longitudinal strain can predict disease progression.
A cute myocarditis is defined as an inflamma- tory reaction in the myocardium, characterized by intense immune cell infiltration.This condition can be triggered by a plethora of factors, including some viral infections and immune checkpoint inhibition therapy, and exhibit a heterogenous presentation and progression. 1Whereas acute myocardial inflammation can sometimes be a self-limiting process, a persistent accumulation of immune cells in the myocardium is linked to chronic inflammatory cardiomyopathy (iCMP) and poor prognosis.Yet, the mechanisms governing the transition from acute myocarditis to progressive iCMP remain poorly understood. 1 Over the course of the last 40 years, numerous studies from independent research groups have established myosin heavy chain alpha (MYHCA, a product of Myh6, the primary cardiac isoform in mice) as a dominant cardiac antigen linked to the development of acute myocarditis in genetically susceptible mouse strains. 2-4Early observations reported an increased production of myosin-specific
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Rizakou et al. (2026) conducted an editorial in Acute myocarditis and inflammatory cardiomyopathy (iCMP). Myosin-specific CD4+ T cells drive progressive inflammatory cardiomyopathy in TCRM mice, while global longitudinal strain at 6 weeks predicts disease progression.
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