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Targeting TET3 in macrophages provides a concept strategy for the treatment of endometriosis
Hossein Hosseinirad, … , Md Saidur Rahman, Jae-Wook Jeong
Hossein Hosseinirad, … , Md Saidur Rahman, Jae-Wook Jeong
Published November 1, 2024
Citation Information: J Clin Invest. 2024;134(21):e185421. https://doi.org/10.1172/JCI185421.
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Commentary

Targeting TET3 in macrophages provides a concept strategy for the treatment of endometriosis

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Abstract

Endometriosis, characterized by the presence of endometrial-like tissue outside the uterus, is a condition associated with pain and infertility. In this issue of the JCI, Lv et al. illuminate the critical pathophysiological role of the ten-eleven translocation 3 (TET3) in endometriosis. TET3 expression levels were higher in macrophages of endometriotic lesions compared with control endometrial tissue, implicating TET3 as a contributing factor in the chronic inflammation that occurs in endometriosis. TGF-β1 and MCP1 are present in the peritoneal cavity of women with endometriosis, and macrophage exposure to these factors resulted in upregulation of TET3, thereby promoting their survival. Notably, Bobcat339, a selective TET inhibitor, induced apoptosis in these macrophages. Further, myeloid-specific TET3 loss reduced endometriosis in mice. RNA-Seq analysis following TET3 knockdown revealed alterations in cytokine signaling and cell-death pathways, underscoring the therapeutic potential of targeting TET3 in macrophages as a strategy for managing endometriosis.

Authors

Hossein Hosseinirad, Md Saidur Rahman, Jae-Wook Jeong

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