Myocardial inflammation in myocarditis: mechanisms and therapeutic targets

Myocarditis is an inflammatory disease of the myocardium with heterogeneous aetiologies, in which innate and adaptive immune responses critically influence clinical outcomes, ranging from complete recovery to progression toward dilated cardiomyopathy. In viral myocarditis, pathogen- and damage-associated molecular patterns activate pattern-recognition receptors, triggering NF-κB and inflammasome signaling and amplifying pro-inflammatory cytokine responses. Early myocardial injury involves neutrophils, mast cells, natural killer cells, and inflammatory monocytes, followed by activation of adaptive immune responses. Imbalance of Th1/Th2 immunity and dysregulation of the Th17/Treg axis promote persistent inflammation and fibrotic remodeling. Autoimmune mechanisms driven by molecular mimicry, pathogenic autoantibodies, and genetic susceptibility further sustain myocardial injury. While conventional biomarkers support diagnosis, emerging inflammatory markers and immune-derived indices show promise for risk stratification and disease monitoring. Beyond guideline-directed heart failure therapy, targeted immunomodulatory strategies are under investigation, highlighting the need for precision approaches to prevent chronic inflammation and adverse remodeling.