Myocarditis is a polymorphic disease complicated with indeterminate etiology and pathogenesis, and represents one of the most challenging clinical problems lacking specific diagnosis and effective
therapy. It is caused by a complex interplay of environmental and genetic factors, and causal links between dysregulated microribonucleic
acids (
miRNAs) and
myocarditis have also been supported by recent epigenetic researches. Both dysregulated CD4+ T cells and
miRNAs play critical roles in the pathogenesis of
myocarditis, and the classic triphasic model of its pathogenesis consists of the acute infectious, subacute immune, and recovery/chronic myopathic phase. CD4+ T cells are key pathogenic factors underlying the development and progression of
myocarditis, and the effector and regulatory subsets, respectively, promote and inhibit autoimmune responses. Furthermore, the reciprocal interplay of these subsets influences the pathogenesis as well. Dysregulated
miRNAs along with their
mRNA and
protein targets have been identified in heart biopsies (intracellular
miRNAs) and body fluids (circulating
miRNAs) during
myocarditis. These
miRNAs show phase-dependent changes, and correlate with
viral infection, immune status,
fibrosis, destruction of cardiomyocytes,
arrhythmias, cardiac functions, and outcomes. Thus,
miRNAs are promising diagnostic markers and therapeutic targets in
myocarditis. In this review, we review
myocarditis with an emphasis on its pathogenesis, and present a summary of current knowledge of dysregulated CD4+ T cells and
miRNAs in
myocarditis.