Our previous mechanistic studies also reported that miR-150 directly and functionally inhibited multiple profibrotic proteins, including HOXA4 and SPRR1A, such that the increased fibrotic markers in adult mice or primary human CFs lacking miR-150 led to sustained activation of CFs, increased MF density, and exacerbated cardiac fibrosis during ischemia [17,18]. This evidence concerns the gene SPRR1A and ischemia.