李春刚, 严双琴, 陶芳标. 妊娠期镉暴露致新生儿端粒长度缩短和儿童心血管代谢健康损害的研究进展[J]. 环境与职业医学, 2023, 40(9): 1085-1089, 1094. DOI: 10.11836/JEOM23046
引用本文: 李春刚, 严双琴, 陶芳标. 妊娠期镉暴露致新生儿端粒长度缩短和儿童心血管代谢健康损害的研究进展[J]. 环境与职业医学, 2023, 40(9): 1085-1089, 1094. DOI: 10.11836/JEOM23046
LI Chungang, YAN Shuangqin, TAO Fangbiao. Research progress on shortened telomere length in newborns and impaired cardiovascular metabolic health in children caused by exposure to cadmium during pregnancy[J]. Journal of Environmental and Occupational Medicine, 2023, 40(9): 1085-1089, 1094. DOI: 10.11836/JEOM23046
Citation: LI Chungang, YAN Shuangqin, TAO Fangbiao. Research progress on shortened telomere length in newborns and impaired cardiovascular metabolic health in children caused by exposure to cadmium during pregnancy[J]. Journal of Environmental and Occupational Medicine, 2023, 40(9): 1085-1089, 1094. DOI: 10.11836/JEOM23046

妊娠期镉暴露致新生儿端粒长度缩短和儿童心血管代谢健康损害的研究进展

Research progress on shortened telomere length in newborns and impaired cardiovascular metabolic health in children caused by exposure to cadmium during pregnancy

  • 摘要:

    妊娠期镉暴露是一个不可忽视的公共卫生问题,可能增加新生儿端粒长度缩短和儿童心血管代谢健康损害的风险,近年来受到诸多研究者关注。本文回顾了近年来国内外有关妊娠期镉暴露、新生儿端粒长度缩短和儿童心血管代谢异常三者关联的研究,简述了妊娠期镉暴露导致新生儿端粒长度缩短的可能机制。目前研究结果指出,妊娠期镉暴露与新生儿端粒长度缩短和儿童心血管代谢异常有关,并且新生儿端粒长度缩短也与儿童心血管代谢异常有关,表明新生儿端粒长度可能是反映妊娠期镉暴露导致儿童心血管代谢异常的生物标志物。另外,妊娠期镉暴露加速新生儿端粒长度缩短的机制包括炎症反应、线粒体功能障碍、抗氧化剂消耗/抗氧化酶失活和DNA甲基化等,这些生物学机制通过某些因子与儿童心血管代谢异常相关联,包括肥胖、血压偏高、空腹血糖受损、血脂异常,提示儿童心血管代谢异常可能在生命早期就被规划,但相关研究仍然较少。未来应进一步研究妊娠期镉暴露、端粒长度和子代心血管代谢三者的关联,同时研究端粒长度在其中的中介效能和相关生物学机制,从而为预防心血管代谢性疾病提供早期生物学信息。

     

    Abstract:

    Cadmium exposure during pregnancy is a non-negligible public health problem which may increase the risk of shortened telomere length in newborns and cardiovascular metabolic health damage in children, and has attracted attention from many researchers in recent years. This article reviewed recent studies both domestically and internationally on the associations among cadmium exposure during pregnancy, shortened telomere length in newborns, and cardiovascular metabolic abnormalities in children, and briefly outlined possible mechanisms of shortened telomere length in newborns by cadmium exposure during pregnancy. Current research results showed that cadmium exposure during pregnancy is related to shortened telomere length in newborns and cardiovascular metabolic abnormalities in children, and shortened telomere length in newborns is also related to cardiovascular metabolic abnormalities in children. It suggested that telomere length in newborns may be a biomarker reflecting cardiovascular metabolic abnormalities in children caused by cadmium exposure during pregnancy. In addition, the current potential mechanisms of cadmium exposure during pregnancy accelerating neonatal telomere length shortening include inflammatory reaction, mitochondrial dysfunction, antioxidant consumption/antioxidant enzyme inactivation, and DNA methylation, and these biological mechanisms are associated with cardiovascular metabolic abnormalities through certain factors, such as obesity, elevated blood pressure, impaired fasting blood glucose, and dyslipidemia in children, suggesting that cardiovascular metabolic abnormalities in children may be programmed in early life, but there are still few relevant studies. In the future, research should be conducted on the association among cadmium exposure during pregnancy, telomere length, and offspring cardiovascular metabolism, as well as possible mediating efficacy and related biological mechanisms of telomere length, aiming to provide early-life biological information for the prevention of cardiovascular and metabolic diseases.

     

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