Role of the axis IL-6/STAT3/complement in regulating chronic inflammation and heart auto-immunity
Prof.ssa Valeria Poli (Pricipal Investigator)
We have shown that STAT3 is both sufficient and necessary to trigger the onset of immune-mediated myocarditis, activating a feed-forward loop involving enhanced IL-6 signalling and complement factors production in the liver (Camporeale et al., 2013). Recently, we have demonstrated that in vivo siRNA-mediated interference with STAT3 or Complement C3 expression in the liver can prevent the onset of experimental myocarditis as well as act therapeutically, opening a window of opportunity for novel precision therapy approaches for this complex disease (Avalle et al., 2020). Current reserch, funded by the Health Ministry (Ricerca Finalizzata) aims at testing several inhibitors of STAT3 activation such as JAK kinases inhibitors, already approved or under clinical trial for different kinds of deseases, in a drug repurposing effort, and at assessing the value of dosing complement activation to predict disease progression. |
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