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    Area of Science:

    • Reproductive Biology
    • Endocrinology
    • Cellular and Molecular Biology

    Background:

    • The uterine endometrium regenerates monthly, regulated by estrogen and progesterone.
    • Obesity disrupts hormonal balance, increasing endometrial hyperplasia (EH) risk due to suppressed progesterone and chronic estrogen exposure.

    Purpose of the Study:

    • To investigate how obesity alters endometrial cell states and contributes to endometrial hyperplasia.
    • To define the molecular mechanisms linking high-fat diet (HFD) to endometrial changes.

    Main Methods:

    • Single-cell RNA sequencing and tissue phenotyping of endometrial tissues from control and EH-predisposed mice on control or HFD.
    • Analysis of fibroblast reprogramming, macrophage recruitment, and epithelial cell signatures.
    • Investigating the role of Estrogen Receptor alpha (ERα) in stromal cells.

    Main Results:

    • HFD reprogrammed endometrial stroma to an inflammatory, pro-fibrotic state, altering fibroblast populations (reducing Aldh1a2⁺, expanding Gsn⁺).
    • HFD impaired macrophage recruitment and promoted hyperplastic epithelial signatures, worsening EH in a mouse model.
    • Stromal ERα deletion confirmed estrogen signaling drives HFD-induced extracellular matrix (ECM) accumulation.

    Conclusions:

    • HFD-driven fibroblast reprogramming is a key mechanism linking estrogen dominance to stromal fibrosis, impaired immune clearance, and increased EH susceptibility.
    • Fibroblast-mediated ECM remodeling in response to progesterone is crucial for normal endometrial homeostasis.