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.
Titolo: | Liver-Specific siRNA-Mediated Stat3 or C3 Knockdown Improves the Outcome of Experimental Autoimmune Myocarditis | |
Autori Riconosciuti: | ||
Autori: | 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. | |
Data di pubblicazione: | 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. | |
Volume: | 18 | |
Pagina iniziale: | 62 | |
Pagina finale: | 72 | |
Digital Object Identifier (DOI): | 10.1016/j.omtm.2020.05.023 | |
Parole Chiave: | acute-phase response (APR); C3/C5 null mice; complement; constitutively active STAT3 mice; experimental autoimmune myocarditis (EAM); hepatotropic siRNA therapy; STAT3 | |
Rivista: | MOLECULAR THERAPY. METHODS & CLINICAL DEVELOPMENT | |
Appare nelle tipologie: | 03A-Articolo su Rivista |
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