ArticleBMC molecular and cell biology2022
Decreased Krüppel-like factor 4 in adenomyosis impairs decidualization by repressing autophagy in human endometrial stromal cells.
Article in BMC molecular and cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 13 citations in OpenAlex.
- Early modulation of autophagy-associated markers in murine adenomyosis and selective persistence in human stromal lesions.Frontiers in endocrinology · 2026Article
- Transcriptional regulation of autophagy in skeletal muscle stem cells.Disease models & mechanisms · 2025Review
- Controversial Roles of Autophagy in Adenomyosis and Its Implications for Fertility Outcomes-A Systematic Review.Journal of clinical medicine · 2024Review
- Dysregulation of CREB5 Impairs Decidualization and Maternal-Fetal Interactions by Inhibiting Autophagy in Recurrent Spontaneous Abortion.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Molecular mechanism of aberrant decidualization in adenomyosis leading to reduced endometrial receptivity.Frontiers in endocrinology · 2024Review
- Exploration the global single-cell ecological landscape of adenomyosis-related cell clusters by single-cell RNA sequencing.Frontiers in genetics · 2022Article
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10 authors at 3 institutions in 1 country.
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Abstract
backgroundPoor decidualization and abnormal autophagy conditions in the endometria of adenomyosis patients have been reported previously. However, the specific regulatory mechanism of decidualization in adenomyosis and its relationship with autophagy levels have not been clarified.
methodsEndometrial tissues from adenomyosis patients and uteri from an adenomyosis mouse model were collected for the detection of different expression patterns of KLF4 and autophagy markers (LC3-B/LC3-A and Beclin-1) compared with control groups. Human endometrial stromal cells (hESCs) isolated from adenomyosis and control endometrial tissues were employed to elucidate the biological functions of KLF4 in autophagy and decidualization. Gene expression regulation was examined by quantitative real-time PCR (qRT-PCR), western blotting and luciferase reporter assays. In addition, DNA promoter-protein interactions were examined by chromatin immunoprecipitation (ChIP)/PCR assay and avidin-biotin conjugate DNA precipitation (ABCD) assay.
resultsKLF4 expression was decreased in endometrial tissues from adenomyosis patients compared with those from fertile controls, especially in stromal compartments. The opposite results were observed for autophagy marker (LC3-B/LC3-A and Beclin-1) expression. At the same time, KLF4 reversed the poor decidualization of hESCs from adenomyosis patients. In addition, KLF4 could induce hESC decidualization by promoting the autophagy level. Mechanistically, KLF4 bound to a conserved site in the autophagy-related 5 (ATG5) promoter region and promoted ATG5 expression. Similar expression patterns of KLF4 and autophagy markers were detected in adenomyotic mice.
conclusionsKLF4 overexpression increases the autophagy level of hESCs by transcriptionally promoting ATG5 expression, and abnormally decreased KLF4 in adenomyosis impairs hESC decidualization by repressing autophagy.
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