In experimental autoimmune myocarditis, chronic activation of the STAT3-IL-6 axis in the liver sustains heart inflammation via complement C3/C5 upregulation. Poli and colleagues demonstrate that lipidoid-siRNA nanoparticles triggering liver-specific STAT3 or C3 silencing represent a therapeutic option, potentially bypassing the side effects of systemic STAT3 or complement inhibition.
Liver-Specific siRNA-Mediated Stat3 or C3 Knockdown Improves the Outcome of Experimental Autoimmune Myocarditis
Avalle L.First
;Marino F.;Camporeale A.;Guglielmi C.;Viavattene D.;Bandini S.;Conti L.;Cimino J.;Forni M.;Zanini C.;Ghigo A.;Cavallo F.;Provero P.;Poli V.Last
2020-01-01
Abstract
In experimental autoimmune myocarditis, chronic activation of the STAT3-IL-6 axis in the liver sustains heart inflammation via complement C3/C5 upregulation. Poli and colleagues demonstrate that lipidoid-siRNA nanoparticles triggering liver-specific STAT3 or C3 silencing represent a therapeutic option, potentially bypassing the side effects of systemic STAT3 or complement inhibition.
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