TLR2 and cardiac hypertrophy: It has been demonstrated that HMGB1 and TLR2 were co-localized in cardiac fibroblasts, accelerated the expressions of α-SMA and Col-1 and subsequently promoted cardiac fibrosis by inhibiting autophagy flux in the cardiac fibroblasts from the isoproterenol-induced myocardial hypertrophy-related cardiac fibrosis mouse model, which was prevented by silencing TLR2 136.