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Decidua

Anatomy and Physiology · NLM MeSH · updated 2026-10-31 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

The hormone-responsive glandular layer of endometrium that sloughs off at each menstrual flow (decidua menstrualis) or at the termination of pregnancy.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (646 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

The hormone-responsive glandular layer of endometrium that sloughs off at each menstrual flow (decidua menstrualis) or at the termination of pregnancy. During pregnancy, the thickest part of the decidua forms the maternal portion of the placenta, thus named decidua placentalis. The thin portion of the decidua covering the rest of the embryo is the decidua capsularis.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Deciduas; Deciduum.

Where it fits in the MeSH classification

Broader topics
Endometrium; Placenta
Narrower topics
Deciduoma

Related concepts

  • Endometrium
  • Placenta

Research landscape

PubMed indexes 6,911 records tagged with the MeSH heading “Decidua” (counts retrieved 2026-10-31). 1,121 of them (16.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,079 records.

Reviews account for 606 records (8.8%) and meta-analyses for 3. Randomized controlled trials number 11 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.

PubMed records by publication periodthrough 1999: 3,079 records; 2000-2009: 1,271 records; 2010-2019: 1,440 records; 2020 onward: 1,121 records3,079through 19991,2712000-20091,4402010-20191,1212020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19993,079
2000-20091,271
2010-20191,440
2020 onward1,121
Share of records by publication typeReviews: 8.8 percent; Meta-analyses: 0.0 percent; Randomized controlled trials: 0.2 percentReviews8.8% (606)Meta-analyses0.0% (3)Randomized controlled trials0.2% (11)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 6,911 PubMed records
TypeRecordsShare
Reviews6068.8%
Meta-analyses30.0%
Randomized controlled trials110.2%

Method: PubMed query "Decidua"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.

Reading the evidence in anatomy and physiology

Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Dynamic Function and Composition Changes of Immune Cells During Normal and Pathological Pregnancy at the Maternal-Fetal Interface
Yang F, Zheng Q, Jin L
2019Review article
Design not recorded in structured metadata
351cc by
PMID 31681264 · DOI · PMC6813251
Endometrial Decidualization: The Primary Driver of Pregnancy Health
Ng SW, Norwitz GA, Pavlicev M, Tilburgs T, Simón C, Norwitz ER
2020Review article
Design not recorded in structured metadata
268cc by
PMID 32521725 · DOI · PMC7312091
Clearance of senescent decidual cells by uterine natural killer cells in cycling human endometrium
Brighton PJ, Maruyama Y, Fishwick K, Vrljicak P, Tewary S, Fujihara R, et al.
2017Research article
Design not recorded in structured metadata
264cc by
PMID 29227245 · DOI · PMC5724991
Single-cell mapping of human endometrium and decidua reveals epithelial and stromal contributions to fertility
Burns GW, Paul EN, Persaud M, Zhao Q, Li R, Blackledge K, et al.
2026Research article
Design not recorded in structured metadata
8cc by
PMID 41574608 · DOI · PMC12892900

Dynamic Function and Composition Changes of Immune Cells During Normal and Pathological Pregnancy at the Maternal-Fetal Interface [1]

Review article Yang F, Zheng Q, Jin L · · 2019 · cited 351 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
A successful pregnancy requires a fine-tuned and highly regulated balance between immune activation and embryonic antigen tolerance.
Closing excerpt
This review summarizes information from previous studies, which may lay the foundation for the diagnosis of pathological pregnancy and put forward new ideas for future studies.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (196 words)

A successful pregnancy requires a fine-tuned and highly regulated balance between immune activation and embryonic antigen tolerance. Since the fetus is semi-allogeneic, the maternal immune system should exert tolerant to the fetus while maintaining the defense against infection. The maternal-fetal interface consists of different immune cells, such as decidual natural killer (dNK) cells, macrophages, T cells, dendritic cells, B cells, and NKT cells. The interaction between immune cells, decidual stromal cells, and trophoblasts constitute a vast network of cellular connections. A cellular immunological imbalance may lead to adverse pregnancy outcomes, such as recurrent spontaneous abortion, pre-eclampsia, pre-term birth, intrauterine growth restriction, and infection. Dynamic changes in immune cells at the maternal-fetal interface have not been clearly stated. While many studies have described changes in the proportions of immune cells in the normal maternal-fetus interface during early pregnancy, few studies have assessed the immune cell changes in mid and late pregnancy. Research on pathological pregnancy has provided clues about these dynamic changes, but a deeper understanding of these changes is necessary. This review summarizes information from previous studies, which may lay the foundation for the diagnosis of pathological pregnancy and put forward new ideas for future studies.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31681264 · DOI · PMC6813251

Endometrial Decidualization: The Primary Driver of Pregnancy Health [2]

Review article Ng SW, Norwitz GA, Pavlicev M, Tilburgs T, Simón C, Norwitz ER · · 2020 · cited 268 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Interventions to prevent pregnancy complications have been largely unsuccessful.
Closing excerpt
We hypothesize, therefore, that the primary driver of pregnancy health is the quality of the soil, not the seed.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (140 words)

Interventions to prevent pregnancy complications have been largely unsuccessful. We suggest this is because the foundation for a healthy pregnancy is laid prior to the establishment of the pregnancy at the time of endometrial decidualization. Humans are one of only a few mammalian viviparous species in which decidualization begins during the latter half of each menstrual cycle and is therefore independent of the conceptus. Failure to adequately prepare (decidualize) the endometrium hormonally, biochemically, and immunologically in anticipation of the approaching blastocyst-including the downregulation of genes involved in the pro- inflammatory response and resisting tissue invasion along with the increased expression of genes that promote angiogenesis, foster immune tolerance, and facilitate tissue invasion-leads to abnormal implantation/placentation and ultimately to adverse pregnancy outcome. We hypothesize, therefore, that the primary driver of pregnancy health is the quality of the soil, not the seed.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32521725 · DOI · PMC7312091

Clearance of senescent decidual cells by uterine natural killer cells in cycling human endometrium [3]

Research article Brighton PJ, Maruyama Y, Fishwick K, Vrljicak P, Tewary S, Fujihara R, et al. · · 2017 · cited 264 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
In cycling human endometrium, menstruation is followed by rapid estrogen-dependent growth.
Closing excerpt
Our findings reveal that acute decidual senescence governs endometrial rejuvenation and remodeling at embryo implantation, and suggest a critical role for uNK cells in maintaining homeostasis in cycling endometrium.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)

In cycling human endometrium, menstruation is followed by rapid estrogen-dependent growth. Upon ovulation, progesterone and rising cellular cAMP levels activate the transcription factor Forkhead box O1 (FOXO1) in endometrial stromal cells (EnSCs), leading to cell cycle exit and differentiation into decidual cells that control embryo implantation. Here we show that FOXO1 also causes acute senescence of a subpopulation of decidualizing EnSCs in an IL-8 dependent manner. Selective depletion or enrichment of this subpopulation revealed that decidual senescence drives the transient inflammatory response associated with endometrial receptivity. Further, senescent cells prevent differentiation of endometrial mesenchymal stem cells in decidualizing cultures. As the cycle progresses, IL-15 activated uterine natural killer (uNK) cells selectively target and clear senescent decidual cells through granule exocytosis. Our findings reveal that acute decidual senescence governs endometrial rejuvenation and remodeling at embryo implantation, and suggest a critical role for uNK cells in maintaining homeostasis in cycling endometrium.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29227245 · DOI · PMC5724991

Single-cell mapping of human endometrium and decidua reveals epithelial and stromal contributions to fertility [4]

Research article Burns GW, Paul EN, Persaud M, Zhao Q, Li R, Blackledge K, et al. · · 2026 · cited 8 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
The human endometrium undergoes dynamic changes across the menstrual cycle to establish a receptive state for embryo implantation.
Closing excerpt
Together, these findings provide a high-resolution transcriptomic atlas of the receptive and early pregnant endometrium and shed light on key molecular pathways underlying successful implantation.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (161 words)

The human endometrium undergoes dynamic changes across the menstrual cycle to establish a receptive state for embryo implantation. Using bulk and single-cell RNA-Seq, we characterized gene expression dynamics in the cycling endometrium and the decidua from early pregnancy. We demonstrated that during the mid-secretory phase - the period encompassing the window of implantation - secretory glandular epithelial cells undergo notable transcriptional changes and alterations in cell-cell communication. Through comprehensive analyses, we identified the glandular epithelium receptivity module (GERM) signature, comprising 556 genes associated with endometrial receptivity. This GERM signature was consistently perturbed across datasets of endometrial samples from women with impaired fertility, validating its relevance as a marker of receptivity. In addition to epithelial changes, we observed shifts in stromal cell populations, notably involving decidual and senescent subsets, which also play key roles in modulating implantation. Together, these findings provide a high-resolution transcriptomic atlas of the receptive and early pregnant endometrium and shed light on key molecular pathways underlying successful implantation.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41574608 · DOI · PMC12892900

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Mechanisms of implantation: strategies for successful pregnancy [5]
    Cha J, Sun X, Dey SK · Nat Med · 2012 · cited 1,061 times (Europe PMC)
  • Research article Cyclic decidualization of the human endometrium in reproductive health and failure [6]
    Gellersen B, Brosens JJ · Endocr Rev · 2014 · cited 873 times (Europe PMC)
  • Research article Immune responses at the maternal-fetal interface [7]
    Ander SE, Diamond MS, Coyne CB · Sci Immunol · 2019 · cited 512 times (Europe PMC)
  • Research article Decidualization of the human endometrium: mechanisms, functions, and clinical perspectives [8]
    Gellersen B, Brosens IA, Brosens JJ · Semin Reprod Med · 2007 · cited 453 times (Europe PMC)
  • Research article Chronic inflammation of the placenta: definition, classification, pathogenesis, and clinical significance [9]
    Kim CJ, Romero R, Chaemsaithong P, Chaemsaithong P, Kim JS · Am J Obstet Gynecol · 2015 · cited 404 times (Europe PMC)
  • Research article The role of decidual immune cells on human pregnancy [10]
    Liu S, Diao L, Huang C, Li Y, Zeng Y, Kwak-Kim JYH · J Reprod Immunol · 2017 · cited 243 times (Europe PMC)

References

  1. Yang F, Zheng Q, Jin L. Dynamic Function and Composition Changes of Immune Cells During Normal and Pathological Pregnancy at the Maternal-Fetal Interface. . 2019. PMID 31681264 · DOI · PMC6813251
  2. Ng SW, Norwitz GA, Pavlicev M, Tilburgs T, Simón C, Norwitz ER. Endometrial Decidualization: The Primary Driver of Pregnancy Health. . 2020. PMID 32521725 · DOI · PMC7312091
  3. Brighton PJ, Maruyama Y, Fishwick K, Vrljicak P, Tewary S, Fujihara R, et al.. Clearance of senescent decidual cells by uterine natural killer cells in cycling human endometrium. . 2017. PMID 29227245 · DOI · PMC5724991
  4. Burns GW, Paul EN, Persaud M, Zhao Q, Li R, Blackledge K, et al.. Single-cell mapping of human endometrium and decidua reveals epithelial and stromal contributions to fertility. . 2026. PMID 41574608 · DOI · PMC12892900
  5. Cha J, Sun X, Dey SK. Mechanisms of implantation: strategies for successful pregnancy. Nat Med. 2012. PMID 23223073 · DOI · PMC6322836
  6. Gellersen B, Brosens JJ. Cyclic decidualization of the human endometrium in reproductive health and failure. Endocr Rev. 2014. PMID 25141152 · DOI
  7. Ander SE, Diamond MS, Coyne CB. Immune responses at the maternal-fetal interface. Sci Immunol. 2019. PMID 30635356 · DOI · PMC6744611
  8. Gellersen B, Brosens IA, Brosens JJ. Decidualization of the human endometrium: mechanisms, functions, and clinical perspectives. Semin Reprod Med. 2007. PMID 17960529 · DOI
  9. Kim CJ, Romero R, Chaemsaithong P, Chaemsaithong P, Kim JS. Chronic inflammation of the placenta: definition, classification, pathogenesis, and clinical significance. Am J Obstet Gynecol. 2015. PMID 26428503 · DOI · PMC4782598
  10. Liu S, Diao L, Huang C, Li Y, Zeng Y, Kwak-Kim JYH. The role of decidual immune cells on human pregnancy. J Reprod Immunol. 2017. PMID 29055791 · DOI

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-31.

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At a glance

6,911
PubMed records on this heading
16%
published since 2020
606
review articles
11
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

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