Targeting HMGB1 ameliorates cardiac fibrosis through restoring TLR2-mediated autophagy suppression in myocardial fibroblasts

Our study suggests that the interaction between TLR2 and HMGB1 contributes to the pathogenesis of cardiac fibrosis via suppressing fibroblast autophagy, and that inhibiting HMGB1 with GA provides therapeutic benefits for the treatment of fibroproliferative heart diseases.