HMGB1 and myocardial infarction: In contrast, muscle specific miR-206, which has been previously shown to increase acutely after MI [24], was markedly up-regulated in failing hearts (Figure 7A) and, following treatment with HMGB1, it exhibited a ∼4–5-fold additional increase, both in the border zone and in the infarct area (Figure 7A), which represented a ∼20–25 fold increase vs the LV expression level in sham operated mice Additional experiments were performed in vitro to confirm HMGB1 effect on miR-206 expression.