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<p>Recurrent spontaneous abortion (RSA) presents a significant reproductive hurdle, impacting 2–5% of women globally. Despite identification of various aetiological factors, approximately half of all cases remain unexplained. In this study, we delve into the critical role of fibroblast growth factor 7 (FGF7) in RSA, particularly in the realm of impaired endometrial receptivity. Leveraging bioinformatic analyses and experimental approaches involving decidual tissues, as well as human endometrial stromal cells (HESCs) and Ishikawa cells culture, we probe into the regulatory patterns of FGF7 and its impact on essential cellular processes pivotal for endometrial function. Our results reveal a correlation between FGF7 downregulation (decreased by approximately 50%, <i>p</i> &lt; 0.05) and disruptions in HESC proliferation and apoptosis, pivotal aspects of RSA pathogenesis. Notably, we delineate the disruptions in decidualisation processes crucial for successful implantation and pregnancy maintenance under FGF7 suppression. These insights deepen our comprehension of the molecular dynamics underlying impaired endometrial receptivity in RSA, potentially guiding the development of targeted therapies. Our study underscores the therapeutic potential of FGF7 modulation, backed by evidence from related studies on its benefits in tissue regeneration and oxidative stress mitigation.</p>

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Downregulation of fibroblast growth factor 7 impairs endometrial receptivity and decidualisation via extracellular signal-regulated kinase and C-Jun N-Terminal kinase pathways, contributing to recurrent spontaneous abortion

  • 期刊论文

  • 发表日期：

    2026年6月29日

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  • Yaqian Lu,
  • Ruiqing Tong,
  • Nan Wang,
  • Weiqin Zhou,
  • Fei Xia,
  • Yanyu Zhong

摘要

Recurrent spontaneous abortion (RSA) presents a significant reproductive hurdle, impacting 2–5% of women globally. Despite identification of various aetiological factors, approximately half of all cases remain unexplained. In this study, we delve into the critical role of fibroblast growth factor 7 (FGF7) in RSA, particularly in the realm of impaired endometrial receptivity. Leveraging bioinformatic analyses and experimental approaches involving decidual tissues, as well as human endometrial stromal cells (HESCs) and Ishikawa cells culture, we probe into the regulatory patterns of FGF7 and its impact on essential cellular processes pivotal for endometrial function. Our results reveal a correlation between FGF7 downregulation (decreased by approximately 50%, p < 0.05) and disruptions in HESC proliferation and apoptosis, pivotal aspects of RSA pathogenesis. Notably, we delineate the disruptions in decidualisation processes crucial for successful implantation and pregnancy maintenance under FGF7 suppression. These insights deepen our comprehension of the molecular dynamics underlying impaired endometrial receptivity in RSA, potentially guiding the development of targeted therapies. Our study underscores the therapeutic potential of FGF7 modulation, backed by evidence from related studies on its benefits in tissue regeneration and oxidative stress mitigation.