Scholarlink

<p>Telomere length (TL) is important for maintaining the individual health of a species. Recent studies shows that in vitro fertilization therapy can drastically reduce TL in offspring, however, the underlying molecular mechanism remains unknown. Sirt6 is a NAD<sup>+</sup>-dependent epigenetic regulator that has recently been found to play an important role in maintaining telomere stability. Here, we report that NAD<sup>+</sup> deficiency in in vitro-cultured blastocysts impairs Sirt6 function, triggering telomere shortening of the inner cell mass and possibly affecting newborns. This phenotype could be effectively mitigated by supplementation with nicotinamide mononucleotide (NAD<sup>+</sup> precursor) during in vitro culture, while it could not be achieved in Sirt6 conditional knockout embryos. mtROS accumulation and epigenetic modifications may also be involved in this process. Our results reveal the mechanism by which in vitro culture induces telomere shortening in preimplantation embryos, providing a potential target for improving in vitro culture conditions.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

NAD+-dependent Sirt6 is a key regulator involved in telomere shortening of in vitro-cultured preimplantation embryos

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年8月23日

查看全文
  • Danjun Li,
  • Wenzhi Li,
  • Xiaoyu Liao,
  • Shutian Jiang,
  • Meng Ma,
  • Zhijie Hu,
  • Kaibo Lin,
  • Weina Yu,
  • Xue Sun,
  • Yong Fan,
  • Haibo Wu,
  • Mingru Yin,
  • Li Wang,
  • Lun Suo,
  • Hui Long,
  • Xuefeng Lu,
  • Yanping Kuang,
  • Qifeng Lyu

摘要

Telomere length (TL) is important for maintaining the individual health of a species. Recent studies shows that in vitro fertilization therapy can drastically reduce TL in offspring, however, the underlying molecular mechanism remains unknown. Sirt6 is a NAD+-dependent epigenetic regulator that has recently been found to play an important role in maintaining telomere stability. Here, we report that NAD+ deficiency in in vitro-cultured blastocysts impairs Sirt6 function, triggering telomere shortening of the inner cell mass and possibly affecting newborns. This phenotype could be effectively mitigated by supplementation with nicotinamide mononucleotide (NAD+ precursor) during in vitro culture, while it could not be achieved in Sirt6 conditional knockout embryos. mtROS accumulation and epigenetic modifications may also be involved in this process. Our results reveal the mechanism by which in vitro culture induces telomere shortening in preimplantation embryos, providing a potential target for improving in vitro culture conditions.