Therefore, in the present work, we attempted to explore (1) whether high-level HMGB1 in EAM was a direct risk factor of myocardial fibrosis; (2) except for immune cells, endothelial cells, cardiomyocytes and necrosis cells, whether cardiac fibroblasts/myofibroblasts, as another important component of heart, were also the critical sources of high-level HMGB1 in EAM. Here, HMGB1 is linked to Myocardial fibrosis.