孕产妇的肥胖引起了后代的代谢障碍和通过表观遗传调节的髓状细胞重编程
Joo Young Kweon1, Hyeonji Mun1, Myeong Ryeol Choi1
1Medical Science and Engineering, Graduate School of Convergence Science and Technology, Pohang University of Science and Technology, Pohang, Republic of Korea.
Frontiers in endocrinology
|January 31, 2024
概括
孕产妇肥胖和妊娠期糖尿病会导致孩子在以后的生活中发展肥胖和心血管问题. 这发生在生命早期通过免疫重编程,受子宫内环境的影响.
科学领域:
- 生殖生物学 生殖生物学
- 发育生物学是发展生物学.
- 免疫学 免疫学 免疫学
背景情况:
- 孕产妇肥胖和妊娠期糖尿病与不利的儿童健康结果有关.
- 早期暴露于代谢不平衡的环境会影响慢性疾病的易感性.
- 对于代谢障碍的母亲出生的孕期大 (LGA) 儿童面临更高的风险.
研究的目的:
- 审查早期生命代谢环境暴露的临床和实验研究.
- 总结母亲肥胖和妊娠糖尿病在儿童肥胖和心血管风险中的作用.
- 探索子宫内环境驱动的髓状细胞重编程和表观遗传机制.
主要方法:
- 对现有的临床和实验研究进行全面审查.
- 分析数据,将母亲的代谢状态与后代的健康联系起来.
- 检查涉及免疫重编程的表观遗传规则和标记物.
主要成果:
- 暴露于孕产妇肥胖和妊娠期糖尿病可能导致LGA儿童.
- 不良的子宫内环境对胎儿的免疫系统进行了重新编程,增加了对肥胖,动脉样硬化,高血压和NAFLD的易感性.
- 表观遗传机制在子宫内环境驱动的髓状细胞重编程中起着至关重要的作用.
结论:
- 由于不良子宫内环境的早期免疫重编程,导致慢性炎症疾病和代谢综合征.
- 表观遗传修饰是关键的潜在机制,将母亲的代谢障碍与后代的长期健康联系起来.
- 对母胎免疫调节和表观遗传机制的进一步研究对于预防肥胖和心血管疾病是有必要的.
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