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 (486 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
The development of anatomical structures to create the form of a single- or multi-cell organism. Morphogenesis provides form changes of a part, parts, or the whole organism.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Where it fits in the MeSH classification
- Broader topics
- Growth and Development
- Narrower topics
- Body Patterning; Embryonic and Fetal Development; Metamorphosis, Biological
Research landscape
PubMed indexes 472,846 records tagged with the MeSH heading “Morphogenesis” (counts retrieved 2026-10-31). 96,482 of them (20.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 153,375 records.
Reviews account for 49,361 records (10.4%) and meta-analyses for 1,226. Randomized controlled trials number 4,402 (0.9%) 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 | 127,028 |
| 2000-2009 | 95,961 |
| 2010-2019 | 153,375 |
| 2020 onward | 96,482 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 49,361 | 10.4% |
| Meta-analyses | 1,226 | 0.3% |
| Randomized controlled trials | 4,402 | 0.9% |
Method: PubMed query "Morphogenesis"[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 |
|---|---|---|---|---|
| Asymmetric distribution of mitochondrial Ca2+ regulators specifies compartment-specific mitochondrial function and neuronal development | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42557311 · DOI · PMC13538658 |
| ATP13A4 gates extracellular polyamine levels to control excitatory synaptogenesis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42680725 · DOI · PMC13534584 |
| CellCover defines marker gene panels capturing developmental progression in neocortical neural stem cell identity | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42517345 · DOI · PMC13412324 |
Asymmetric distribution of mitochondrial Ca2+ regulators specifies compartment-specific mitochondrial function and neuronal development [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Neuronal polarization is essential for functional compartmentalization, enabling dendritic synaptic integration and axonal action potential generation.
- Closing excerpt
- These findings highlight fundamental Ca2+-modulating features and developmental importance of neuronal mitochondria in a compartment-specific manner and reveal the key underlying molecular determinants.
- 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 (150 words)
Neuronal polarization is essential for functional compartmentalization, enabling dendritic synaptic integration and axonal action potential generation. Although structural differences in mitochondria across compartments have been identified, their functional distinctions remain unclear. Here, we uncovered compartment-specific mitochondrial Ca2+ dynamics and their molecular determinants. In axonal mitochondria, Ca2+ uptake through mitochondrial Ca2+ uniporter occurs independently of ER-stored Ca2+ release, with faster matrix Ca2+ clearance than dendritic mitochondria, where Ca2+ uptake predominantly originates from ER Ca2+. The ER-independent mitochondrial Ca2+ uptake in axonal mitochondria is associated with enriched mitochondrial Ca2+ uniporter-regulating proteins, MICU1 and MICU2, whereas higher NCLX expression facilitates rapid Ca2+ clearance. Moreover, NCLX knockdown, which functionally mimics a mental retardation-associated mutation, caused more significant developmental defects of axons than dendrites in vivo, aligning with its enrichment in axons. These findings highlight fundamental Ca2+-modulating features and developmental importance of neuronal mitochondria in a compartment-specific manner and reveal the key underlying molecular determinants.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42557311 · DOI · PMC13538658
ATP13A4 gates extracellular polyamine levels to control excitatory synaptogenesis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Polyamines, such as spermidine, are essential regulators of brain development, yet how cells control their uptake and extracellular levels remains unclear.
- Closing excerpt
- Thus, astrocytic polyamine clearance via ATP13A4 tunes extracellular spermidine to shape synapse formation during development.
- 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 (153 words)
Polyamines, such as spermidine, are essential regulators of brain development, yet how cells control their uptake and extracellular levels remains unclear. Here we show that ATP13A4, a transport protein enriched in glia and prominently expressed in astrocytes, governs brain polyamine balance. Using biochemical, cellular, and animal models, we find that ATP13A4 imports polyamines into cells and thereby limits their availability outside cells. Loss of ATP13A4 simplifies astrocyte morphology and increases the excitatory connections, or synapses, that astrocytes promote between neurons; adding spermidine reproduces these effects, identifying extracellular spermidine as a synapse-promoting signal. In mice lacking Atp13a4, brain polyamines are redistributed, with reduced levels in the cortex and accumulation in cerebrospinal fluid. This is accompanied by excess excitatory synapses, delayed early development, and mild, female-biased behavioral changes in adulthood. Rare ATP13A4 variants linked to neurodevelopmental disorders disrupt its function. Thus, astrocytic polyamine clearance via ATP13A4 tunes extracellular spermidine to shape synapse formation during development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42680725 · DOI · PMC13534584
CellCover defines marker gene panels capturing developmental progression in neocortical neural stem cell identity [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Defining cell classes is central to the analysis of growing single-cell RNA sequencing (scRNA-seq) atlases.
- Closing excerpt
- Examining outer radial glia markers across mammals, we find that transcriptomic elements of this key cell type likely arose in rodent gliogenic precursors before the full program emerged in the primate lineage.
- 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 (183 words)
Defining cell classes is central to the analysis of growing single-cell RNA sequencing (scRNA-seq) atlases. Marker genes are most often identified by differential expression (DE) methods that assess genes one at a time, ignoring the redundancy and complementarity revealed when genes are considered jointly. Working with binarized expression data, we instead seek discriminating panels of genes that together are specific to a cell type, framing marker-panel selection as a variant of the minimal set-covering problem in combinatorial optimization. This formulation efficiently searches the vast space of candidate panels, exploits the large cell numbers typical of scRNA-seq, and is robust to zero-inflation. Using blood and brain data, we show that our method, CellCover, reduces gene redundancy and captures cell-class-specific signals distinct from those found by DE. Transfer-learning experiments across mouse, primate, and human data demonstrate that CellCover identifies conserved cell classes in neocortical neurogenesis and tracks developmental progression in progenitors and neurons. Examining outer radial glia markers across mammals, we find that transcriptomic elements of this key cell type likely arose in rodent gliogenic precursors before the full program emerged in the primate lineage.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42517345 · DOI · PMC13412324
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 Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis [4]
- Research article Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth [5]
- Research article Aspirin for the prevention of preterm and term preeclampsia: systematic review and metaanalysis [6]
- Research article Gestational weight gain across continents and ethnicity: systematic review and meta-analysis of maternal and infant outcomes in more than one million women [7]
- Research article Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth [8]
- Research article Preterm birth and the metabolic syndrome in adult life: a systematic review and meta-analysis [9]
References
- Jang DC, Kim SY, Kim WS, Choi IY, Jang E, Jung H, et al.. Asymmetric distribution of mitochondrial Ca2+ regulators specifies compartment-specific mitochondrial function and neuronal development. . 2026. PMID 42557311 · DOI · PMC13538658
- van Veen S, Meeus E, Irala D, Sakers K, Liu Z, Savage J, et al.. ATP13A4 gates extracellular polyamine levels to control excitatory synaptogenesis. . 2026. PMID 42680725 · DOI · PMC13534584
- Ji L, Wang A, Sonthalia S, Seo S, Naiman DQ, Younes L, et al.. CellCover defines marker gene panels capturing developmental progression in neocortical neural stem cell identity. . 2026. PMID 42517345 · DOI · PMC13412324
- Cermak NM, Res PT, de Groot LC, Saris WH, van Loon LJ. Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis. Am J Clin Nutr. 2012. PMID 23134885 · DOI
- Roberts D, Brown J, Medley N, Dalziel SR. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2017. PMID 28321847 · DOI · PMC6464568
- Roberge S, Bujold E, Nicolaides KH. Aspirin for the prevention of preterm and term preeclampsia: systematic review and metaanalysis. Am J Obstet Gynecol. 2018. PMID 29138036 · DOI
- Goldstein RF, Abell SK, Ranasinha S, Misso ML, Boyle JA, Harrison CL, et al.. Gestational weight gain across continents and ethnicity: systematic review and meta-analysis of maternal and infant outcomes in more than one million women. BMC Med. 2018. PMID 30165842 · DOI · PMC6117916
- McGoldrick E, Stewart F, Parker R, Dalziel SR. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2020. PMID 33368142 · DOI · PMC8094626
- Parkinson JR, Hyde MJ, Gale C, Santhakumaran S, Modi N. Preterm birth and the metabolic syndrome in adult life: a systematic review and meta-analysis. Pediatrics. 2013. PMID 23509172 · 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.