ArticleReproductive sciences (Thousand Oaks, Calif.)2023
PIM2 Promotes the Development of Ovarian Endometriosis by Enhancing Glycolysis and Fibrosis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- The role of fibrosis in endometriosis: a systematic review.Human reproduction update · 2024Pooled it
- Aberrant mitochondria in endometriosis: From pathogenic mechanisms to therapeutic opportunities.iScience · 2026Review
- Lactate and lactylation: mechanisms, function, diseases, and therapeutic targets.Molecular biomedicine · 2026Review
- BDNF facilitates ectopic endometrial stromal cell growth, invasion, migration and glycolysis in endometriosis via upregulating GLUT1.CytoJournal · 2026Article
- PRMT3-mediated FOXO1 arginine methylation exacerbates oxidative stress-induced decidualization defects in the eutopic endometrium of endometriosis.Cellular and molecular life sciences : CMLS · 2025Article
- Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3-Regulated HIF1A/HMOX1 Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Warburg-like Metabolic Reprogramming in Endometriosis: From Molecular Mechanisms to Therapeutic Approaches.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Endometriosis and Cytoskeletal Remodeling: The Functional Role of Actin-Binding Proteins.Cells · 2025Review
- NEK2 promotes the development of ovarian endometriosis and impairs decidualization by phosphorylating FOXO1.Cellular and molecular life sciences : CMLS · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.