SFRP4+ stromal cell subpopulation with IGF1 signaling in human endometrial regeneration

Bingbing Wu, Li Yu, Nanfang Nie, Xilin Shen, Wei Jiang, Yanshan Liu, Lin Gong, Chengrui An, Kun Zhao, Xudong Yao, Chunhui Yuan, Jinghui Hu, Wei Zhao, Jianhua Qian, Xiaohui Zou
In: Cell Discovery · 2022 · vol. 8(1) , pp. 95 · doi:10.1038/s41421-022-00438-7 · PMID:36163341 · W4297100812
article OA: gold CC0 ⤵ 5 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

Researchers identified an SFRP4+ stromal cell subpopulation in the human uterus that enhances endometrial regeneration via IGF1 signaling.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-06 ⓘ

Using droplet-based single-cell RNA sequencing of full-thickness human uterine tissue from seven donors across proliferative and secretory menstrual phases (10,551 filtered cells), Wu et al. mapped cell heterogeneity and inferred cell population architectures, identifying six main cell types and 20 subpopulations. They found an SFRP4+ stromal subpopulation highly enriched in the regenerative stage, and showed that SFRP4+ stromal cells enhanced proliferation of human endometrial epithelial organoids in vitro and promoted endometrial epithelial gland regeneration and recovery from full-thickness endometrial injury in vivo through IGF1 signaling. A key limitation is that the study uses human tissue sampled at two menstrual phases and relies on computational integration/clustering plus in vitro and in vivo functional assays to assign regenerative roles to a specific stromal subset. This paper is centrally about endometriosis — it provides endometrial regenerative biology (SFRP4+ stromal/IGF1-driven repair) that is relevant to how pelvic endometrial tissue might remodel or fail to regenerate in endometriosis-associated pathology, despite not being primarily focused on endometriosis itself.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Abstract Our understanding of full-thickness endometrial regeneration after injury is limited by an incomplete molecular characterization of the cell populations responsible for the organ functions. To help fill this knowledge gap, we characterized 10,551 cells of full-thickness normal human uterine from two menstrual phases (proliferative and secretory phase) using unbiased single cell RNA-sequencing. We dissected cell heterogeneity of main cell types (epithelial, stromal, endothelial, and immune cells) of the full thickness uterine tissues, cell population architectures of human uterus cells across the menstrual cycle. We identified an SFRP4 + stromal cell subpopulation that was highly enriched in the regenerative stage of the human endometria during the menstrual cycle, and the SFRP4 + stromal cells could significantly enhance the proliferation of human endometrial epithelial organoid in vitro, and promote the regeneration of endometrial epithelial glands and full-thickness endometrial injury through IGF1 signaling pathway in vivo. Our cell atlas of full-thickness uterine tissues revealed the cellular heterogeneities, cell population architectures, and their cell–cell communications during the monthly regeneration of the human endometria, which provide insight into the biology of human endometrial regeneration and the development of regenerative medicine treatments against endometrial damage and intrauterine adhesion.

My notes (saved in your browser only)

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (39)

Cited by (5)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK