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 (602 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 development of the placenta, a highly vascularized mammalian fetal-maternal organ and major site of transport of oxygen, nutrients, and fetal waste products between mother and fetus. The process begins at fertilization, through the development of cytotrophoblasts and syncytiotrophoblasts, the formation of chorionic villi, to the progressive increase in blood vessels to support the growing fetus.
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: Placental Development; Hemochorial Placentation; Placentation, Hemochorial; Hemochorial Placental Development; Placental Development, Hemochorial.
Where it fits in the MeSH classification
- Broader topics
- Pregnancy
Related concepts
- Placenta
- Fetus
- Fertilization
- Trophoblasts
- Trophoblasts
- Chorionic Villi
- Blood Vessels
Research landscape
PubMed indexes 3,523 records tagged with the MeSH heading “Placentation” (counts retrieved 2026-10-31). 898 of them (25.5%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,390 records.
Reviews account for 886 records (25.1%) and meta-analyses for 15. Randomized controlled trials number 17 (0.5%) 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.
Show the data
| Period | Records |
|---|---|
| through 1999 | 536 |
| 2000-2009 | 699 |
| 2010-2019 | 1,390 |
| 2020 onward | 898 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 886 | 25.1% |
| Meta-analyses | 15 | 0.4% |
| Randomized controlled trials | 17 | 0.5% |
Method: PubMed query "Placentation"[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 / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Single-cell RNA-seq reveals the diversity of trophoblast subtypes and patterns of differentiation in the human placenta | 2018 | Research article Design not recorded in structured metadata | 370 | cc by PMID 30042384 · DOI · PMC6082907 |
| Uterine glands coordinate on-time embryo implantation and impact endometrial decidualization for pregnancy success | 2018 | Research article Design not recorded in structured metadata | 155 | cc by PMID 29934619 · DOI · PMC6015089 |
| The Role of Epigenetics in Placental Development and the Etiology of Preeclampsia | 2019 | Review article Design not recorded in structured metadata | 147 | cc by PMID 31212604 · DOI · PMC6600551 |
| Platelets link coagulation and complement in regulating murine placental vascular development | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42490403 · DOI · PMC13574145 |
Single-cell RNA-seq reveals the diversity of trophoblast subtypes and patterns of differentiation in the human placenta [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The placenta is crucial for a successful pregnancy and the health of both the fetus and the pregnant woman.
- Closing excerpt
- These results document human placental trophoblast differentiation at single-cell resolution and thus advance our understanding of human placentation during the early stage of pregnancy.
- 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 (156 words)
The placenta is crucial for a successful pregnancy and the health of both the fetus and the pregnant woman. However, how the human trophoblast lineage is regulated, including the categorization of the placental cell subtypes is poorly understood. Here we performed single-cell RNA sequencing (RNA-seq) on sorted placental cells from first- and second-trimester human placentas. New subtypes of cells of the known cytotrophoblast cells (CTBs), extravillous trophoblast cells (EVTs), Hofbauer cells, and mesenchymal stromal cells were identified and cell-type-specific gene signatures were defined. Functionally, this study revealed many previously unknown functions of the human placenta. Notably, 102 polypeptide hormone genes were found to be expressed by various subtypes of placental cells, which suggests a complex and significant role of these hormones in regulating fetal growth and adaptations of maternal physiology to pregnancy. These results document human placental trophoblast differentiation at single-cell resolution and thus advance our understanding of human placentation during the early stage of pregnancy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30042384 · DOI · PMC6082907
Uterine glands coordinate on-time embryo implantation and impact endometrial decidualization for pregnancy success [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Uterine glands are essential for pregnancy establishment.
- Closing excerpt
- These studies provide evidence that uterine glands synchronize embryo-endometrial interactions, coordinate on-time embryo implantation, and impact stromal cell decidualization, thereby ensuring embryo viability, placental growth, and pregnancy success.
- 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 (137 words)
Uterine glands are essential for pregnancy establishment. By employing forkhead box A2 (FOXA2)-deficient mouse models coupled with leukemia inhibitory factor (LIF) repletion, we reveal definitive roles of uterine glands in embryo implantation and stromal cell decidualization. Here we report that LIF from the uterine glands initiates embryo-uterine communication, leading to embryo attachment and stromal cell decidualization. Detailed histological and molecular analyses discovered that implantation crypt formation does not involve uterine glands, but removal of the luminal epithelium is delayed and subsequent decidualization fails in LIF-replaced glandless but not gland-containing FOXA2-deficient mice. Adverse ripple effects of those dysregulated events in the glandless uterus result in embryo resorption and pregnancy failure. These studies provide evidence that uterine glands synchronize embryo-endometrial interactions, coordinate on-time embryo implantation, and impact stromal cell decidualization, thereby ensuring embryo viability, placental growth, and pregnancy success.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29934619 · DOI · PMC6015089
The Role of Epigenetics in Placental Development and the Etiology of Preeclampsia [3]
Abstract reading summary — source excerpts
- Opening excerpt
- In this review, we comprehensively present the function of epigenetic regulations in normal placental development as well as in a prominent disease of placental origin, preeclampsia (PE).
- Closing excerpt
- The correlation between epigenetic marks and impacts on gene expression is systematically evaluated for the different epigenetic marks analyzed.
- 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 (120 words)
In this review, we comprehensively present the function of epigenetic regulations in normal placental development as well as in a prominent disease of placental origin, preeclampsia (PE). We describe current progress concerning the impact of DNA methylation, non-coding RNA (with a special emphasis on long non-coding RNA (lncRNA) and microRNA (miRNA)) and more marginally histone post-translational modifications, in the processes leading to normal and abnormal placental function. We also explore the potential use of epigenetic marks circulating in the maternal blood flow as putative biomarkers able to prognosticate the onset of PE, as well as classifying it according to its severity. The correlation between epigenetic marks and impacts on gene expression is systematically evaluated for the different epigenetic marks analyzed.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31212604 · DOI · PMC6600551
Platelets link coagulation and complement in regulating murine placental vascular development [4]
Abstract reading summary — source excerpts
- Opening excerpt
- During early pregnancy, maternal blood surrounds the embryo before the placenta is fully developed, requiring tight regulation of maternal blood flow into the placental vasculature.
- Closing excerpt
- Successful pregnancy therefore requires not only activation but also tight regulation of these systems to balance necessary PMT formation with the prevention of pathological thrombosis.
- 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 (189 words)
During early pregnancy, maternal blood surrounds the embryo before the placenta is fully developed, requiring tight regulation of maternal blood flow into the placental vasculature. We identify placental microthrombi (PMTs) as essential structures guiding this process. PMTs contain platelets, coagulation factors, and complement proteins, and their formation depends on maternal platelet activation by thrombin through the protease-activated receptor 4 (PAR4). Deficiency of PAR4 abolished PMTs and caused excessive bleeding at the implantation site. C3 deficiency also led to increased bleeding events, indicating that complement activation contributes to thrombosis in the placental circulation. Conversely, dysregulated complement activation in CMP-sialic acid synthase-deficient (Cmas-/-) mice led to widespread thrombosis and failed placental development. Strikingly, platelet activation via PAR4 was necessary to localize complement activation to trophoblast surfaces, thereby coupling coagulation and complement in PMT formation. Depletion of maternal platelets mitigated complement-driven thromboinflammation in Cmas-/- pregnancies, restoring placental growth. These findings uncover a critical cooperation between platelets, coagulation, and complement in establishing maternal blood flow to the placenta. Successful pregnancy therefore requires not only activation but also tight regulation of these systems to balance necessary PMT formation with the prevention of pathological thrombosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42490403 · DOI · PMC13574145
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 Preeclampsia: Pathophysiology, Challenges, and Perspectives [5]
- Research article Mechanisms of implantation: strategies for successful pregnancy [6]
- Research article Pathophysiology of placental-derived fetal growth restriction [7]
- Research article Development of the human placenta [8]
- Research article Paleovirology of 'syncytins', retroviral env genes exapted for a role in placentation [9]
- Research article Tracking placental development in health and disease [10]
References
- Liu Y, Fan X, Wang R, Lu X, Dang YL, Wang H, et al.. Single-cell RNA-seq reveals the diversity of trophoblast subtypes and patterns of differentiation in the human placenta. . 2018. PMID 30042384 · DOI · PMC6082907
- Kelleher AM, Milano-Foster J, Behura SK, Spencer TE. Uterine glands coordinate on-time embryo implantation and impact endometrial decidualization for pregnancy success. . 2018. PMID 29934619 · DOI · PMC6015089
- Apicella C, Ruano CSM, Méhats C, Miralles F, Vaiman D. The Role of Epigenetics in Placental Development and the Etiology of Preeclampsia. . 2019. PMID 31212604 · DOI · PMC6600551
- Smid A, Schumann L, Oleshko O, Peters-Bernard U, Flächsig-Schulz K, Whitehead M, et al.. Platelets link coagulation and complement in regulating murine placental vascular development. . 2026. PMID 42490403 · DOI · PMC13574145
- Rana S, Lemoine E, Granger JP, Karumanchi SA. Preeclampsia: Pathophysiology, Challenges, and Perspectives. Circ Res. 2019. PMID 30920918 · DOI
- Cha J, Sun X, Dey SK. Mechanisms of implantation: strategies for successful pregnancy. Nat Med. 2012. PMID 23223073 · DOI · PMC6322836
- Burton GJ, Jauniaux E. Pathophysiology of placental-derived fetal growth restriction. Am J Obstet Gynecol. 2018. PMID 29422210 · DOI
- Turco MY, Moffett A. Development of the human placenta. Development. 2019. PMID 31776138 · DOI
- Lavialle C, Cornelis G, Dupressoir A, Esnault C, Heidmann O, Vernochet C, et al.. Paleovirology of 'syncytins', retroviral env genes exapted for a role in placentation. Philos Trans R Soc Lond B Biol Sci. 2013. PMID 23938756 · DOI · PMC3758191
- Aplin JD, Myers JE, Timms K, Westwood M. Tracking placental development in health and disease. Nat Rev Endocrinol. 2020. PMID 32601352 · 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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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.