Trophoblast aging driven by IL33 deficiency elevates recurrent pregnancy loss risk through SNAP29 lactylation-mediated autophagy impairment.

Jia-Jing Lu, Yan-Ran Sheng, Wen-Ting Hu, Yu-Kai Liu, Feng Xie, Ming-Qing Li, Xiao-Yong Zhu

Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Shanghai Medical School, Fudan University, Shanghai, People's Republic of China. · pubmed

Paper

Abstract

Emerging evidence implicates premature placental senescence as a central driver of pregnancy complications, though its underlying mechanisms remain elusive. Here, we report marked downregulation of IL33 (interleukin 33) in villi from unexplained recurrent pregnancy loss (URPL) patients, concomitant with elevated trophoblast senescence. More importantly,

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Research summary

The paper claims that IL33 deficiency leads to trophoblast aging and increased risk of recurrent pregnancy loss through impaired autophagy. This research is relevant as it explores mechanisms of placental senescence, which could contribute to understanding aging processes and their impact on reproductive health.

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