Autophagy markers are dysregulated in the endometrial tissues of patients with unexplained repeated implantation

Yuanchang Zhu1,2, Zhiqin Zhang1, Zhuanhong Ma2

  • 1Fertility Center, Jiangxi Maternal and Child Health Hospital, Nanchang, China.

Insights

Autophagy, a cellular process, is significantly altered in women with recurrent implantation failure (RIF). This study reveals increased autophagy markers in RIF patients, suggesting its role in RIF pathogenesis.

Area of Science:

  • Reproductive biology
  • Cellular and molecular mechanisms
  • Genomics and proteomics

Background:

  • Endometrium decidualization is crucial for pregnancy but its molecular mechanisms, including the role of autophagy, are not fully understood.
  • Recurrent implantation failure (RIF) is a complex condition affecting fertility, with underlying molecular causes needing further elucidation.

Purpose of the Study:

  • To investigate the potential association between autophagy and recurrent implantation failure (RIF).
  • To identify molecular differences in endometrial tissues between RIF patients and controls.

Main Methods:

  • Gene expression analysis identified differentially expressed genes between RIF and control groups.
  • Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were performed.
  • Autophagy markers (LC3-II, LAMP2, HIF-1α, P62) and autophagy puncta were assessed at protein and cellular levels.

Main Results:

  • Significant differences in gene expression were observed, with 81 genes downregulated and 231 genes upregulated in the RIF group (p < 0.05).
  • Key autophagy markers (LC3-II, LAMP2, HIF-1α) were elevated, while P62 was reduced in RIF patients.
  • Enhanced autophagy puncta were detected in the endometrial tissues of RIF patients, consistent with protein-level findings.

Conclusions:

  • Autophagy is significantly associated with recurrent implantation failure.
  • Altered autophagy may play a critical role in the pathogenesis of RIF, highlighting a potential therapeutic target.