In non-ischemic cardiomyopathy, inflammation is closely associated with cardiac fibrosis, which significantly contributes to adverse outcomes and promotes heart failure (HF). Recent mechanistic studies have demonstrated that interactions between fibrotic and inflammatory pathways create a dynamic, self-perpetuating fibroinflammatory loop, thereby accelerating disease progression. New mono or combination therapies that target this cycle by blocking specific inflammatory signals, modulating the immune response, and altering extracellular matrix (ECM) stiffness may halt or even reverse fibrosis. This opinion article discusses critical recent discoveries, current obstacles, and future opportunities in developing inflammation-focused treatments for cardiac fibrosis in non-ischemic cardiomyopathies.
Qiu et al. (Mon,) studied this question.