“…MIRI can also genetically activate intracellular signaling pathways, like mitogen-activated protein kinases (MAPKs), emerging subfamilies of which include p38MAPK and JNK that might trigger the inflammation-apoptosis chain during MIRI by regulating the expression of extracellular regulated kinase (ERK1/2) [119, 120]. Indeed, the detection of the activity of p38MAPK and JNK has been currently designed as a paradigm for estimating the cardioprotective effects against MIRI of the developing therapeutic molecules (e.g., morphine [121], kaempferol [122], febuxostat [123], and triiodothyronine [124]) in the very dimension of gene expression. Accordingly, the overexpression of the upstream downregulatory genes of the MAPK pathway (e.g., DUSP1 [51], DUSP14 [125], and RGS5 [126]) and/or silencing of its up-regulatory genes (e.g., FPR1 [127]) might be useful for preventing MIRI by suppressing cardiac inflammation, cardiomyocyte apoptosis, and ventricular remodeling [126–128].…”