〔Abstract〕 To investigate the effects of C1q tumor necrosis factor-related protein 3 (CTRP3)-enhanced Sendai virus (SeV) vector-overexpressing Gata4 , Mef2c , and Tbx5 (SeVGMT) in the treatment of myocardial in- farction (MI) mice and to analyze whether ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) mediates this thera- peutic pathway. Methods The mice were divided into 7 groups ( n = 12) : Sham group , MI group , SeVGMT group , CTRP3-Lv group , UCHL1-sh group , SeVGMT + CTRP3-Lv group , and SeVGMT + CTRP3-Lv + UCHL1-sh group . In the Sham group , only the skin was incised without ligation , while the coronary artery was ligated 2 - 3 mm below the left atrial appendage in mice in other groups . PBS was injected at three points in the myocardial in- farction boundary in the Sham and MI groups 30 minutes after ligation . Mice in other groups were injected with level of METTL14 mRNA was positively correlated with the level of m6A in placental tissue . The results of the CCK-8 experiment showed that compared with the control group , knockdown of METTL14 expression in trophoblast cells significantly reduced the cell proliferation rate , while the proliferation ability of trophoblast cells with overex- pressed METTL14 was enhanced . The results of the scratch test showed that compared with the control group , the relative healing rate of scratches was significantly reduced after METTL14 knockdown , while it increased after the overexpression of METTL14 . The results of the Transwell assay and invasion assay showed that compared with the control group , after knockdown of METTL14 , the number of trophoblast cells passing through the chamber was sig- nificantly reduced , while the number of trophoblast cells with overexpressed METTL14 passing through the chamber increased . Conclusion The total RNA m6A modification level in placental tissue of ePE is lower than that in the normal pregnancy group . The down-regulation of methyltransferase METTL14 is involved in the regulation of the to- tal RNA m6A modification level . The overexpression of METTL14 can enhance the proliferation , migration and in- vasion abilities of trophoblast cells . It provides a new perspective for exploring the pathogenesis of early-onset pre- eclampsia.