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: 3 complete abstracts (510 words), 9 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
A post-morula preimplantation mammalian embryo that develops from a 32-cell stage into a fluid-filled hollow ball of over a hundred cells. A blastocyst has two distinctive tissues. The outer layer of trophoblasts gives rise to extra-embryonic tissues. The inner cell mass gives rise to the embryonic disc and eventual embryo proper.
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: Blastocysts; Embryo, Preimplantation; Embryos, Preimplantation; Preimplantation Embryo; Preimplantation Embryos.
Where it fits in the MeSH classification
- Broader topics
- Embryo, Mammalian
- Narrower topics
- Blastocyst Inner Cell Mass; Trophoblasts
Related concepts
Research landscape
PubMed indexes 34,386 records tagged with the MeSH heading “Blastocyst” (counts retrieved 2026-10-31). 7,604 of them (22.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 10,078 records.
Reviews account for 3,233 records (9.4%) and meta-analyses for 78. Randomized controlled trials number 207 (0.6%) 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 | 10,078 |
| 2000-2009 | 7,469 |
| 2010-2019 | 9,235 |
| 2020 onward | 7,604 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,233 | 9.4% |
| Meta-analyses | 78 | 0.2% |
| Randomized controlled trials | 207 | 0.6% |
Method: PubMed query "Blastocyst"[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 |
|---|---|---|---|---|
| Mechano-osmotic signals control chromatin state and fate transitions in pluripotent stem cells | 2025 | Research article Design not recorded in structured metadata | 27 | cc by PMID 41023488 · DOI · PMC12527910 |
| Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst | 2025 | Research article Design not recorded in structured metadata | 17 | cc by PMID 40721412 · DOI · PMC12304225 |
| Live imaging of late-stage preimplantation human embryos reveals de novo mitotic errors | 2026 | Research article Design not recorded in structured metadata | 14 | cc by PMID 41131150 · DOI · PMC7618924 |
Mechano-osmotic signals control chromatin state and fate transitions in pluripotent stem cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Acquisition of specific cell shapes and morphologies is a central component of cell fate transitions.
- Closing excerpt
- Our findings uncover a critical mechanochemical feedback mechanism that integrates nuclear mechanics, shape and volume with biochemical signalling and chromatin state to control cell fate transition dynamics.
- 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 (201 words)
Acquisition of specific cell shapes and morphologies is a central component of cell fate transitions. Although signalling circuits and gene regulatory networks that regulate pluripotent stem cell differentiation have been intensely studied, how these networks are integrated in space and time with morphological changes and mechanical deformations to control state transitions remains a fundamental open question. Here we focus on two distinct models of pluripotency, preimplantation inner cell mass cells of human embryos and primed pluripotent stem cells, to discover that cell fate transitions associate with rapid, compaction-triggered changes in nuclear shape and volume. These phenotypical changes and the associated active deformation of the nuclear envelope arise from growth factor signalling-controlled changes in cytoskeletal confinement and chromatin mechanics. The resulting osmotic stress state triggers global transcriptional repression, macromolecular crowding and remodelling of nuclear condensates that prime chromatin for a cell fate transition by attenuating repression of differentiation genes. However, while this mechano-osmotic chromatin priming has the potential to accelerate fate transitions and differentiation, sustained biochemical signals are required for robust induction of specific lineages. Our findings uncover a critical mechanochemical feedback mechanism that integrates nuclear mechanics, shape and volume with biochemical signalling and chromatin state to control cell fate transition dynamics.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41023488 · DOI · PMC12527910
Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Studies in the mouse demonstrate the importance of fibroblast growth factor (FGF) and extra-cellular receptor tyrosine kinase (ERK) in specification of embryo-fated epiblast and yolk-sac-fated hypoblast cells from uncommitted inner cell mass (ICM) cells prior to implantation.
- Closing excerpt
- Our functional study demonstrates the molecular mechanisms governing ICM specification in human development, whereby segregation of the epiblast and hypoblast lineages occurs during maturation of the mammalian embryo in an ERK signal-dependent manner.
- 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 (146 words)
Studies in the mouse demonstrate the importance of fibroblast growth factor (FGF) and extra-cellular receptor tyrosine kinase (ERK) in specification of embryo-fated epiblast and yolk-sac-fated hypoblast cells from uncommitted inner cell mass (ICM) cells prior to implantation. Molecular mechanisms regulating specification of early lineages in human development are comparatively unclear. Here we show that exogenous FGF stimulation leads to expanded hypoblast molecular marker expression, at the expense of the epiblast. Conversely, we show that specifically inhibiting ERK activity leads to expansion of epiblast cells functionally capable of giving rise to naïve human pluripotent stem cells. Single-cell transcriptomic analysis indicates that these epiblast cells downregulate FGF signalling and maintain molecular markers of the epiblast. Our functional study demonstrates the molecular mechanisms governing ICM specification in human development, whereby segregation of the epiblast and hypoblast lineages occurs during maturation of the mammalian embryo in an ERK signal-dependent manner.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40721412 · DOI · PMC12304225
Live imaging of late-stage preimplantation human embryos reveals de novo mitotic errors [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Existing methods to image chromosome segregation errors are not suitable for studying human embryos at advanced preimplantation stages.
- Closing excerpt
- Our findings raise questions about clinical uses of preimplantation genetic testing for aneuploidy, while providing broadly applicable imaging and segmentation methods for studying diverse cellular structures in human embryos.
- 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 (163 words)
Existing methods to image chromosome segregation errors are not suitable for studying human embryos at advanced preimplantation stages. As chromosomal errors are a leading cause of miscarriage and infertility, it remains unclear whether missegregation arises postfertilization. Here we optimize nuclear DNA labeling via messenger RNA electroporation and apply light-sheet live imaging to reveal chromosome segregation errors immediately before implantation. We show that embryos at advanced preimplantation stages display missegregation, including multipolar spindle formation, lagging chromosomes, misalignment and mitotic slippage. Most lagging chromosomes are passively inherited rather than reincorporated. To trace individual nuclei, we developed an open-source, semi-automated segmentation method using a customized deep learning model optimized for variability in embryo size, shape and signal. With this approach, we find most labeled cells remain externally positioned, consistent with placental rather than inner cell mass fate. Our findings raise questions about clinical uses of preimplantation genetic testing for aneuploidy, while providing broadly applicable imaging and segmentation methods for studying diverse cellular structures in human embryos.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41131150 · DOI · PMC7618924
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 Human placenta and trophoblast development: key molecular mechanisms and model systems [4]
- Research article Development of the human placenta [5]
- Research article The two-stage placental model of preeclampsia: An update [6]
- Research article Mechanisms of early placental development in mouse and humans [7]
- Research article Dynamic Function and Composition Changes of Immune Cells During Normal and Pathological Pregnancy at the Maternal-Fetal Interface [8]
- Research article Syncytiotrophoblast stress in preeclampsia: the convergence point for multiple pathways [9]
References
- McCreery KP, Stubb A, Stephens R, Fursova NA, Cook A, Kruse K, et al.. Mechano-osmotic signals control chromatin state and fate transitions in pluripotent stem cells. . 2025. PMID 41023488 · DOI · PMC12527910
- Simon CS, McCarthy A, Woods L, Staneva D, Proks M, Salehin N, et al.. Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst. . 2025. PMID 40721412 · DOI · PMC12304225
- Abdelbaki A, McCarthy A, Karsa A, Muresan L, Elder K, Papathanasiou A, et al.. Live imaging of late-stage preimplantation human embryos reveals de novo mitotic errors. . 2026. PMID 41131150 · DOI · PMC7618924
- Knöfler M, Haider S, Saleh L, Pollheimer J, Gamage TKJB, James J. Human placenta and trophoblast development: key molecular mechanisms and model systems. Cell Mol Life Sci. 2019. PMID 31049600 · DOI · PMC6697717
- Turco MY, Moffett A. Development of the human placenta. Development. 2019. PMID 31776138 · DOI
- Staff AC. The two-stage placental model of preeclampsia: An update. J Reprod Immunol. 2019. PMID 31301487 · DOI
- Hemberger M, Hanna CW, Dean W. Mechanisms of early placental development in mouse and humans. Nat Rev Genet. 2020. PMID 31534202 · DOI
- Yang F, Zheng Q, Jin L. Dynamic Function and Composition Changes of Immune Cells During Normal and Pathological Pregnancy at the Maternal-Fetal Interface. Front Immunol. 2019. PMID 31681264 · DOI · PMC6813251
- Redman CWG, Staff AC, Roberts JM. Syncytiotrophoblast stress in preeclampsia: the convergence point for multiple pathways. Am J Obstet Gynecol. 2022. PMID 33546842 · 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.