“…Experiments show that expression of FAP (fibroblast activation protein alpha) [66], THBS4 [67], CD27 [68], LEF1 [69], CTHRC1 [70], ESR1 [71], CXCL9 [72], SERPINA3 [73], TRPC4 [74], F13A1 [75], PIK3C2A [76], KCNIP2 [77] and GPR4 [78] contributed to myocardial infarction. MFAP4 [79], ALOX15 [80], COL1A1 [81], APOA1 [82], PDE5A [83], CX3CR1 [84], THY1 [85], GREM1 [86], FMOD (fibromodulin) [87], NPPA (natriuretic peptide A) [88], LTBP2 [89], LUM (lumican) [90], IL34 [91], NRG1 [92], CXCL14 [93], CXCL10 [94], ACE (angiotensin I converting enzyme) [95], CFTR (ystic fibrosis transmembrane conductance regulator) [96], S100A8 [97], S100A9 [97], HP (haptoglobin) [98] [162], Zhang et al [163] and Chen et al [164] study indicated that the expression of CCL22, CCR1, FPR1, KNG1, CRISPLD2, CD38 and GPRC5A were linked with progression of ischemic heart disease. Li et al [165] showed that STEAP3 expression can be associated with cardiac hypertrophy progression.…”