Therapeutically Targetable Th17-Derived miR-721 Drives Autoimmune Myocarditis.

Blocking mmu-miR-721 in experimental autoimmune myocarditis mice increases Pparg, lowers RORγt/IL-17 activity, reduces cardiac leukocyte infiltration, and improves cardiac function.

• Why it matters: Myocarditis therapies are nonspecific, and the disease-relevant role of Th17-derived miR-721 in both mouse models and human patients is unclear.
• What they did: The study detected mmu-miR-721 and hsa-RNA-Chr8:96 in extracellular vesicles from Th17 cells in IL-17 eGFP mice and myocarditis patients, validated Pparg/PPARG targeting, then used lentiviral overexpression, miRNA sponges, and in vivo miR-721 blockade.
• The result: miR-721 overexpression promoted Th17 differentiation via Pparg inhibition, while blockade reversed this pathway and ameliorated disease progression in mice, supporting miR-721 as a therapeutic target.

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