ArticleThe Journal of clinical investigation2025
ZMIZ1 and estrogen receptor α form an essential partnership in endometrial biology.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Glycomic Insights in Gynecological Disease: From Molecular Mechanisms to Precision Diagnostics and Therapeutics.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Estrogen receptor α (ESR1) is a pivotal regulator of endometrial homeostasis and reproductive function, yet the coregulators that fine tune its transcriptional activity remain incompletely defined. In this issue of the JCI, Hewitt et al. identified Zinc finger MIZ-type containing 1 (ZMIZ1) as an ESR1 coregulator that is essential for stromal proliferation, decidualization, and overall endometrial integrity. ZMIZ1 deficiency was associated with endometriosis and endometrial cancer, and conditional ablation of Zmiz1 using the PgrCre mouse led to infertility and accelerated fibrosis due to impaired estrogen responsiveness. These findings position ZMIZ1 as a key modulator of estrogen signaling with translational potential as both a biomarker and a therapeutic target in uterine disorders.
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Registered trials
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