Figure 2. Prominent progress on the molecular mechanisms of IUA and TE. (IMAGE)
Caption
Left Panel: Top—a schematic diagram illustrating the IUA model. Middle—histological sections stained for EMT markers (E-cadherin and N-cadherin), autophagy markers (LC3B and P62), accompanied by a heatmap showcasing alterations in inflammatory factors in IUA patients, as well as a t-SNE plot derived from single-cell analysis (different colors represent different cell populations). Bottom—a summary of the observed pathological changes in IUA, encompassing epithelial homeostasis imbalance, aberrant epigenetic regulation in both epithelial and stromal cells, autophagy defects, persistent inflammation involving macrophages and T cells, ferroptosis, and myofibroblast activation. Right Panel: Top—a schematic diagram depicting the TE model. Middle—histological sections stained for senescence markers (P16 and Ki67), estrogen receptor (ER), and vascular endothelial growth factor (vWF), accompanied by a t-SNE plot from single-cell analysis (different colors represent different cell populations). Bottom—a summary of the observed pathological changes in TE, including senescence affecting pericytes, stem cells, epithelial cells, and stromal cells, inhibited cell proliferation in stromal cells, and immune cell abnormalities involving NK cells and macrophages.
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