ArticleMolecular endocrinology (Baltimore, Md.)2011
Dehydroepiandrosterone inhibits glucose flux through the pentose phosphate pathway in human and mouse endometrial stromal cells, preventing decidualization and implantation.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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.
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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.
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Who cites it
49 citing papers in PubMed, 85 citations in OpenAlex.
- The role of metabolic reprogramming in oocyte development: research progress and prospects.Frontiers in reproductive health · 2026Review
- Key glycometabolism during oocyte maturation and early embryonic development.Reproduction (Cambridge, England) · 2025Review
- Article
- The role of the pentose phosphate pathway on reproductive functions.Animal reproduction · 2025Review
- Steroid hormone regulation of immunometabolism and inflammation.Frontiers in immunology · 2025Review
- Glucose metabolism and endometrium decidualization.Frontiers in endocrinology · 2025Review
- Review
- Decreased AMPK/SIRT1/PDK4 induced by androgen excess inhibits human endometrial stromal cell decidualization in PCOS.Cellular and molecular life sciences : CMLS · 2024Article
- Prevention of Pregnancy Complications Using a Multimodal Lifestyle, Screening, and Medical Model.Journal of clinical medicine · 2024Review
- Reducing the Risk of Pre-Eclampsia in Women with Polycystic Ovary Syndrome Using a Combination of Pregnancy Screening, Lifestyle, and Medical Management Strategies.Journal of clinical medicine · 2024Review
- A common allele increases endometrial Wnt4 expression, with antagonistic implications for pregnancy, reproductive cancers, and endometriosis.Nature communications · 2024Article
- Endometrial Glucose Metabolism During Early Pregnancy.Reproduction & fertility · 2023Article
- Article
- Energy metabolism and maternal-fetal tolerance working in decidualization.Frontiers in immunology · 2023Review
- Glucose and fatty acids catabolism during in vitro decidualization of human endometrial stromal cells.Journal of assisted reproduction and genetics · 2022Article
- Endometrial glycogen metabolism during early pregnancy in mice.Molecular reproduction and development · 2022Article
- SARS- CoV-2 infection and oxidative stress in early-onset preeclampsia.Biochimica et biophysica acta. Molecular basis of disease · 2022Review
- Fructose-1,6-bisphosphate prevents pregnancy loss by inducing decidual COX-2Science advances · 2022Article
- Current Studies of Mitochondrial Quality Control in the Preeclampsia.Frontiers in cardiovascular medicine · 2022Review
- Expression of SGLT1 in the Mouse Endometrial Epithelium and its Role in Early Embryonic Development and Implantation.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Endometrial stromal cells (ESC) must undergo a hormone-driven differentiation to form decidual cells as a requirement of proper embryo implantation. Recent studies from our laboratory have demonstrated that decidualizing cells require glucose transporter 1 expression and an increase in glucose use to complete this step. The present study focuses on the glucose-dependent molecular and metabolic pathways, which are required by ESC for decidualization. Inhibition of glycolysis had no effect on decidualization. However, blockade of the pentose phosphate pathway (PPP) with pharmacologic inhibitors 6-aminonicotinamide or dehydroepiandrosterone (DHEA), and short hairpin RNA-mediated knockdown of glucose-6-phosphate dehydrogenase, the rate-limiting step in the PPP, both led to strong decreases in decidual marker expression in vitro and decreased decidualization in vivo. Additionally, the studies demonstrate that inhibition is due, at least in part, to ribose-5-phosphate depletion, because exogenous nucleoside administration restored decidualization in these cells. The finding that PPP inhibition prevents decidualization of ESC is novel and clinically important, because DHEA is an endogenous hormone produced by the adrenal glands and elevated in a high proportion of women who have polycystic ovary syndrome, the most common endocrinopathy in reproductive age women. Together, this data suggest a mechanistic link between increased DHEA levels, use of glucose via the PPP, and pregnancy loss.
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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.