Paradoxical role of phosphorylated STAT3 in normal fertility and the pathogenesis of adenomyosis and endometriosis†
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Phosphorylated STAT3 is crucial for normal embryo implantation and decidualization but its excessive activation contributes to adenomyosis and endometriosis progression.
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Abstract
Signal transducer and activator of transcription 3 (STAT3), when phosphorylated at tyrosine 705, plays an important role in endometrial stromal cell decidualization and the receptivity of the endometrial epithelium during embryo implantation. However, the function of phosphorylated STAT3 (p-STAT3) in normal uterine receptivity is distinct from that in adenomyosis and endometriosis. In normal pregnancy, STAT3 phosphorylation in the endometrial epithelium determines the success of embryo implantation by regulating uterine receptivity. Additionally, p-STAT3 promotes cellular proliferation and differentiation during endometrial decidualization, which is crucial for embryonic development. In contrast, excessive STAT3 phosphorylation occurs in adenomyosis and endometriosis, which may lead to disease progression. Therefore, achieving a delicate balance in STAT3 activation is crucial. This review aimed to focus on the current understanding and knowledge gaps regarding the control of p-STAT3 activity in normal and pathological endometrial processes. This topic is important because precise control of p-STAT3 production could alleviate the symptoms of adenomyosis and endometriosis, improve endometrial receptivity, and potentially mitigate infertility without compromising normal fertility processes.
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References (62)
- Aberrant activation of signal transducer and activator of transcription-3 (STAT3) signaling in endometriosis via openalex
- Adenomyosis pathogenesis: insights from next-generation sequencing via openalex
- Constant Activation of STAT3 Contributes to the Development of Adenomyosis in Females via openalex
- Decidualization of the human endometrium via openalex
- Decreased Endometrial IL-10 Impairs Endometrial Receptivity by Downregulating HOXA10 Expression in Women with Adenomyosis via openalex
- Ectopic endometriotic stromal cells-derived lactate induces M2 macrophage polarization via Mettl3/Trib1/ERK/STAT3 signalling pathway in endometriosis via openalex
- Endometrial epithelial ARID1A is critical for uterine gland function in early pregnancy establishment via openalex
- Endometriosis via openalex
- Endometriosis: pathogenesis and treatment via openalex
- Enhanced miR-210 expression promotes the pathogenesis of endometriosis through activation of signal transducer and activator of transcription 3 via openalex
- Gankyrin has a potential role in embryo implantation via activation of STAT3 via openalex
- Hypoxia‐inhibited DUSP2 expression promotes IL‐6/STAT3 signaling in endometriosis via openalex
- Is it time for a paradigm shift in drug research and development in endometriosis/adenomyosis? via openalex
- Macrophages Are Alternatively Activated in Patients with Endometriosis and Required for Growth and Vascularization of Lesions in a Mouse Model of Disease via openalex
- Niclosamide As a Potential Nonsteroidal Therapy for Endometriosis That Preserves Reproductive Function in an Experimental Mouse Model via openalex
- Possible involvement of signal transducer and activator of transcription-3 in cell–cell interactions of peritoneal macrophages and endometrial stromal cells in human endometriosis via openalex
- PROBLEMS IN THE DIAGNOSIS OF ADENOMYOSIS UTERI. WITH SPECIAL REFERENCE TO DYSFUNCTIONAL BLEEDING via openalex
- The co-expression of GPER and Gankyrin in ovarian endometriosis and its correlation with the rASRM stages via openalex
- Tofacitinib alters STAT3 signaling and leads to endometriosis lesion regression via openalex
- W2144680752 via openalex
- W2155628078 via openalex
- W2164499002 via openalex
- W2167917245 via openalex
- W2223140939 via openalex
- W2315545909 via openalex
- W2401206178 via openalex
- W2605112455 via openalex
- W2626842659 via openalex
- W2807148066 via openalex
- W2890934004 via openalex
- W2955680264 via openalex
- W3034800306 via openalex
- W3084052485 via openalex
- W3087992083 via openalex
- W3216146155 via openalex
- W4205977732 via openalex
- W4223422330 via openalex
- W4223555190 via openalex
- W4280491716 via openalex
- W4281859427 via openalex
- W6653886155 via openalex
- W6699205349 via openalex
- W1779691448 via openalex
- W6757840361 via openalex
- W1907769497 via openalex
- W1988917700 via openalex
- W1999821753 via openalex
- W2003673719 via openalex
- W2008025540 via openalex
- W2010939329 via openalex
- W2029275361 via openalex
- W2038036973 via openalex
- W2042794591 via openalex
- W2050606256 via openalex
- W2054928345 via openalex
- W2097219651 via openalex
- W2099578825 via openalex
- W2100872519 via openalex
- W2118597337 via openalex
- W2119975890 via openalex
- W2127365820 via openalex
- W2138483567 via openalex
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- europepmc
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