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

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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acute-phase response (APR); C3/C5 null mice; complement; constitutively active STAT3 mice; experimental autoimmune myocarditis (EAM); hepatotropic siRNA therapy; STAT3
Avalle L.; Marino F.; Camporeale A.; Guglielmi C.; Viavattene D.; Bandini S.; Conti L.; Cimino J.; Forni M.; Zanini C.; Ghigo A.; Bogorad R.L.; Cavallo F.; Provero P.; Koteliansky V.; Poli V.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1765655
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