PIM2 Promotes the Development of Ovarian Endometriosis by Enhancing Glycolysis and Fibrosis

Mengxue Wang, Ruiqi Fan, Junyi Jiang, Fangyuan Sun, Yujun Sun, Qian Wang, Aifang Jiang, Zhenhai Yu, Tingting Yang
Reproductive sciences (Thousand Oaks, Calif.) · 2023 · vol. 30(9) , pp. 2692–2702 · doi:10.1007/s43032-023-01208-w · PMID:37059967 · W4365504429
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

This study found that PIM2 promotes ovarian endometriosis development by enhancing glycolysis and fibrosis via PKM2 upregulation, and PIM2 inhibition reduced endometriosis in mice.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper studied the role and mechanism of the kinase PIM2 in ovarian endometriosis, using immunohistochemistry on ovarian endometriosis tissues and mechanistic experiments in endometriotic cells, along with pharmacologic inhibition and in vivo modeling. The authors report that PIM2, glycolysis-related proteins (including HK2 and PKM2), and fibrosis/mesenchymal markers (SMH, Desmin, and α-SMA) are strongly expressed in ovarian endometriosis, and that in endometriotic cells PIM2 enhances glycolysis and fibrosis by upregulating PKM2; treatment with the PIM2 inhibitor SMI-4a and a PIM2 knockout mouse model both inhibited endometriosis development. A key limitation explicitly implied by the study design is that mechanistic evidence relies on specific biomarkers and pathway modulation rather than fully defined upstream drivers or comprehensive pathway mapping. This paper is centrally about endometriosis — it demonstrates that PIM2 promotes ovarian endometriosis by enhancing glycolysis and fibrosis.

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Abstract

Endometriosis is a common gynecological disorder characterized by the presence of the endometrial glands and the stroma outside the uterine cavity. The disease affects reproductive function and quality of life in women of reproductive age. Endometriosis is similar to tumors in some characteristics, such as glycolysis. PIM2 can promote the development of tumors, but the mechanism of PIM2 in endometriosis is still unclear. Therefore, our goal is to study the mechanism of PIM2 in endometriosis. Through immunohistochemistry, we found PIM2, HK2, PKM2, SMH (smooth muscle myosin heavy chain), Desmin, and α-SMA (α-smooth muscle actin) were strongly expressed in the ovarian endometriosis. In endometriotic cells, PIM2 enhanced glycolysis and fibrosis via upregulating the expression of PKM2. Moreover, the PIM2 inhibitor SMI-4a inhibited the development of endometriosis. And we established a PIM2 knockout mouse model of endometriosis to demonstrate the role of PIM2 in vivo. In summary, our study indicates that PIM2 promotes the development of endometriosis. PIM2 may serve as a promising therapeutic target for endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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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.

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