Why the study?
The pathogenesis of dilated cardiomyopathy remains unknown, but evidence indicates that immune cells and inflammatory cascades play a key role in its development.
This review highlights the immunopathogenesis of dilated cardiomyopathy, emphasizing the role of immune cells and cytokines as potential biomarkers and therapeutic targets.
Dilated cardiomyopathy (DCM) is a non-ischemic cardiomyopathy involving one or more underlying etiologies. It is characterized by structural and functional dysfunction of the myocardium, potentially leading to fibrosis and ventricular remodeling, and an elevated risk of heart failure (HF). Although the pathogenesis of DCM remains unknown, compelling evidence suggests that DCM-triggered immune cells and inflammatory cascades play a crucial role in the occurrence and development of DCM. Various factors are linked to myocardial damage, inducing aberrant activation of the immune system and sustained inflammatory responses in DCM. The investigation of the immunopathogenesis of DCM also contributes to discovering new biomarkers and therapeutic targets. This review examines the roles of immune cells and related cytokines in DCM pathogenesis and explores immunotherapy strategies in DCM.
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Zhang et al. (2024) studied this question.
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