早产儿因摄入不足等原因所致的缺锌可引起心脏发育不全。研究表明，Tbx20基因突变在调控心脏发育进程中起着关键作用，但其翻译后修饰对心脏发育的影响研究甚少。我们预实验发现缺锌通过抑制蛋白的SUMO1修饰诱导心脏异常发育，并初步确定TBX20为SUMO1修饰的靶蛋白，其修饰水平的改变参与缺锌条件下胎鼠房室垫发育不良的发生，但TBX20的SUMO化修饰调控心脏发育不全的分子机制尚需进一步研究。因此，本项目将在E10.5-E18.5胎鼠中检测SUMO家族成员及TBX20蛋白、MT1基因在心脏房室垫发育过程中的时空表达特点；研究缺锌调控TBX20蛋白SUMO化修饰的机理；探索SUMO化TBX20通过调控MT1降低缺锌诱导的心肌细胞氧化应激，对早产儿心脏发育发挥保护作用的分子机制。本研究为临床早产儿心脏发育不全的预防及治疗提供新的靶点和思路，具有重要的理论和临床意义。

Zinc deficiency caused by insufficient intake may induce abnormal heart development of premature infants. Although studies have suggested that mutations in the transcription factor TBX20 are associated with abnormal cardiac development, the effect of Tbx20 post-translational modification on cardiac development remains to be explored. Our previous study found that zinc deficiency induces aberrant cardiac development by inhibiting protein SUMOylation.TBX20 is modified by SUMO1 and TBX20 SUMOylation is involved in cardiac cushion formation defects in fetal rats under zinc deficiency condition. However, the mechanism of TBX20 SUMOylation in fetal cardiomyocytes is not clear. This study will detect the temporal and spatial expressions of SUMO family members, TBX20 and MT1 from embryonic day (E) 9.5 to E18.5 mouse embryos; systematically analyze the SUMOylation sites of TBX20 in zinc deficiency model and explore the protective mechanism of TBX20 SUMOylation in regulating MT1 expression and reducing oxidative stress in heart development of premature infants. The study will provide new targets and ideas for clinical prevention and treatment of abnormal cardiac development in premature infants, which has the important theoretical and clinical significance.