Scholarlink

<p>Gestational diabetes mellitus (GDM) is a pregnancy-associated metabolic disorder characterized by insulin resistance and hyperglycemia, posing significant risks to maternal-fetal health. While placental inflammation contributes to GDM pathology, its cellular mechanisms remain incompletely understood. Leveraging public single-cell RNA sequencing (scRNA-seq) data, we constructed a cellular atlas of GDM and control placental tissues, identifying 14 transcriptionally distinct populations. Neutrophil_1 emerged as the dominant pro-inflammatory subset, exhibiting amplified interactions with macrophages and T cells that exacerbate inflammatory responses. Pseudotime trajectory analysis revealed Neutrophil_2 as a precursor state differentiating toward the Neutrophil_1 lineage through transcriptionally regulated programming. Critically, Arginine catabolism and Nicotinate/nicotinamide metabolism were found to modulate Neutrophil_1’s pro-inflammatory functions. Our findings implicate pathogenic neutrophil subsets in GDM progression and nominate arginase and NAMPT inhibition as potential therapeutic strategies for mitigating neutrophil-mediated placental inflammation.</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

Single-cell sequencing reveals that neutrophils mediate the inflammatory response in the placenta of women with GDM

  • 期刊论文

  • 发表日期：

    2026年1月17日

查看全文
  • Shi Yin,
  • Na Zhuo,
  • Qing Duan,
  • Jinyu Song,
  • Chunrui Yang

摘要

Gestational diabetes mellitus (GDM) is a pregnancy-associated metabolic disorder characterized by insulin resistance and hyperglycemia, posing significant risks to maternal-fetal health. While placental inflammation contributes to GDM pathology, its cellular mechanisms remain incompletely understood. Leveraging public single-cell RNA sequencing (scRNA-seq) data, we constructed a cellular atlas of GDM and control placental tissues, identifying 14 transcriptionally distinct populations. Neutrophil_1 emerged as the dominant pro-inflammatory subset, exhibiting amplified interactions with macrophages and T cells that exacerbate inflammatory responses. Pseudotime trajectory analysis revealed Neutrophil_2 as a precursor state differentiating toward the Neutrophil_1 lineage through transcriptionally regulated programming. Critically, Arginine catabolism and Nicotinate/nicotinamide metabolism were found to modulate Neutrophil_1’s pro-inflammatory functions. Our findings implicate pathogenic neutrophil subsets in GDM progression and nominate arginase and NAMPT inhibition as potential therapeutic strategies for mitigating neutrophil-mediated placental inflammation.