MiR-425-5p intervenes in autoimmune myocarditis by regulating Treg cell differentiation through NRAS

• DOI: 10.3389/fcell.2025.1600103
• Publication Date: 2025-05-13T05:29:22Z
• Authors: Shan Zhou; Li Zhang; Xiuyun Duan; Keyu Liu; You Yingnan; Mengjie Ma; Bo Han
• Keywords: Treg cell

Our Previous research revealed significant differences in exosome-mediated intercellular miR-425a-5p between normal children and those with fulminant myocarditis. We sought to elucidate the molecular underpinnings functional implications of context myocarditis progression. Bioinformatics techniques were employed predict NRAS as target gene miR-425a-5p. constructed a cellular paradigm through LPS-mediated provocation AC16 cardiomyocyte cultures. MiR-425a-5p was overexpressed, expressions NRAS, cell apoptosis, proinflammatory cytokine profiles, encompassing IL-1β, IL-6, TNF-α, comprehensively quantified. An experimental autoimmune (EAM) mouse model created using adeno-associated virus (AAV) for overexpression. Comprehensive histopathological analyses conducted utilizing multiple staining techniques, including hematoxylin-eosin (HE), immunohistochemical, Masson trichrome methodologies characterize tissue responses. The study demonstrated that alleviated inflammatory response both cells EAM mice mediation. Single-cell data analysis cardiac immune promoted Treg differentiation improved function. plays crucial role modulating responses myocarditis, potentially offering novel therapeutic strategy managing disease.