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

ABSTRACT:

Aim

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 and functional implications of miR-425a-5p in the context of myocarditis progression.

Methods

Bioinformatics techniques were employed to predict NRAS as the target gene of miR-425a-5p. We constructed a cellular myocarditis paradigm through LPS-mediated provocation of AC16 cardiomyocyte cultures. MiR-425a-5p was overexpressed, and the expressions of NRAS, cell apoptosis, and proinflammatory cytokine profiles, encompassing IL-1β, IL-6, and TNF-α, were comprehensively quantified. An experimental autoimmune myocarditis (EAM) mouse model was created using adeno-asso

SUBMITTER: Zhou S 

PROVIDER: S-EPMC12106460 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature