Additionally, the upregulation of hypoxia inducible factor-1α (HIF-1α) was triggered by hypoxic conditions during the inflammatory phase, which was related to LBH-induced CF proliferative acceleration [13], whereas CF activation is due to the comprehensive effects of different causes in the post-MI cardiac microenvironment [14], and potential LBH-associated mechanisms regarding the communication between CFs and other cardiac cell types, such as CMs, endothelial cells, inflammatory cells, and immune cells [15], remain largely unclear. Here, CFTR is linked to myocardial infarction.