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 (676 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 narrow subcapsular outer zone of the adrenal cortex. This zone produces a series of enzymes that convert pregnenolone to aldosterone. The final steps involve three successive oxidations by cytochrome p-450 cyp11b2.
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: Glomerulosa, Zona; Adrenal Glomerulosa; Glomerulosa, Adrenal.
Where it fits in the MeSH classification
- Broader topics
- Adrenal Cortex
Related concepts
- Pregnenolone
- Aldosterone
- Cytochrome P-450 Cyp11B2
Research landscape
PubMed indexes 1,008 records tagged with the MeSH heading “Zona Glomerulosa” (counts retrieved 2026-10-31). 56 of them (5.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 642 records.
Reviews account for 59 records (5.9%) and meta-analyses for 0. Randomized controlled trials number 2 (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.
Show the data
| Period | Records |
|---|---|
| through 1999 | 642 |
| 2000-2009 | 185 |
| 2010-2019 | 125 |
| 2020 onward | 56 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 59 | 5.9% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 2 | 0.2% |
Method: PubMed query "Zona Glomerulosa"[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 |
|---|---|---|---|---|
| PKA inhibits WNT signalling in adrenal cortex zonation and prevents malignant tumour development | 2016 | Research article Design not recorded in structured metadata | 101 | cc by PMID 27624192 · DOI · PMC5027289 |
| β-Catenin and FGFR2 regulate postnatal rosette-based adrenocortical morphogenesis | 2020 | Research article Design not recorded in structured metadata | 52 | cc by PMID 32245949 · DOI · PMC7125176 |
| Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism | 2019 | Research article Design not recorded in structured metadata | 44 | cc by PMID 31615979 · DOI · PMC6794291 |
| ClC-2 Contributes to Hypotonicity-Induced Adrenal Aldosterone Secretion | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 41606697 · DOI · PMC12852535 |
PKA inhibits WNT signalling in adrenal cortex zonation and prevents malignant tumour development [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Adrenal cortex physiology relies on functional zonation, essential for production of aldosterone by outer zona glomerulosa (ZG) and glucocorticoids by inner zona fasciculata (ZF).
- Closing excerpt
- These observations suggest that PKA acts as a tumour suppressor in the adrenal cortex, through repression of WNT signalling.
- 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 (151 words)
Adrenal cortex physiology relies on functional zonation, essential for production of aldosterone by outer zona glomerulosa (ZG) and glucocorticoids by inner zona fasciculata (ZF). The cortex undergoes constant cell renewal, involving recruitment of subcapsular progenitors to ZG fate and subsequent lineage conversion to ZF identity. Here we show that WNT4 is an important driver of WNT pathway activation and subsequent ZG differentiation and demonstrate that PKA activation prevents ZG differentiation through WNT4 repression and WNT pathway inhibition. This suggests that PKA activation in ZF is a key driver of WNT inhibition and lineage conversion. Furthermore, we provide evidence that constitutive PKA activation inhibits, whereas partial inactivation of PKA catalytic activity stimulates β-catenin-induced tumorigenesis. Together, both lower PKA activity and higher WNT pathway activity lead to poorer prognosis in adrenocortical carcinoma (ACC) patients. These observations suggest that PKA acts as a tumour suppressor in the adrenal cortex, through repression of WNT signalling.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27624192 · DOI · PMC5027289
β-Catenin and FGFR2 regulate postnatal rosette-based adrenocortical morphogenesis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Rosettes are widely used in epithelial morphogenesis during embryonic development and organogenesis.
- Closing excerpt
- Together, our data provide an example of rosette-mediated postnatal tissue morphogenesis and a framework for studying the role of rosettes in adult zona glomerulosa tissue maintenance and function.
- 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)
Rosettes are widely used in epithelial morphogenesis during embryonic development and organogenesis. However, their role in postnatal development and adult tissue maintenance remains largely unknown. Here, we show zona glomerulosa cells in the adult adrenal cortex organize into rosettes through adherens junction-mediated constriction, and that rosette formation underlies the maturation of adrenal glomerular structure postnatally. Using genetic mouse models, we show loss of β-catenin results in disrupted adherens junctions, reduced rosette number, and dysmorphic glomeruli, whereas β-catenin stabilization leads to increased adherens junction abundance, more rosettes, and glomerular expansion. Furthermore, we uncover numerous known regulators of epithelial morphogenesis enriched in β-catenin-stabilized adrenals. Among these genes, we show Fgfr2 is required for adrenal rosette formation by regulating adherens junction abundance and aggregation. Together, our data provide an example of rosette-mediated postnatal tissue morphogenesis and a framework for studying the role of rosettes in adult zona glomerulosa tissue maintenance and function.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32245949 · DOI · PMC7125176
Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Human primary aldosteronism (PA) can be caused by mutations in several ion channel genes but mouse models replicating this condition are lacking.
- Closing excerpt
- By reproducing essential features of human PA, Clcn2op mice are a valuable model to study the pathological mechanisms underlying this disease.
- 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)
Human primary aldosteronism (PA) can be caused by mutations in several ion channel genes but mouse models replicating this condition are lacking. We now show that almost all known PA-associated CLCN2 mutations markedly increase ClC-2 chloride currents and generate knock-in mice expressing a constitutively open ClC-2 Cl- channel as mouse model for PA. The Clcn2op allele strongly increases the chloride conductance of zona glomerulosa cells, provoking a strong depolarization and increasing cytoplasmic Ca2+ concentration. Clcn2op mice display typical features of human PA, including high serum aldosterone in the presence of low renin activity, marked hypertension and hypokalemia. These symptoms are more pronounced in homozygous Clcn2op/op than in heterozygous Clcn2+/op mice. This difference is attributed to the unexpected finding that only ~50 % of Clcn2+/op zona glomerulosa cells are depolarized. By reproducing essential features of human PA, Clcn2op mice are a valuable model to study the pathological mechanisms underlying this disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31615979 · DOI · PMC6794291
ClC-2 Contributes to Hypotonicity-Induced Adrenal Aldosterone Secretion [4]
Abstract reading summary — source excerpts
- Opening excerpt
- AimThe zona glomerulosa (ZG) of the adrenal cortex regulates blood pressure and electrolyte homeostasis through aldosterone production.
- Closing excerpt
- These data advance our understanding of regulators of aldosterone production.
- 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 (226 words)
AimThe zona glomerulosa (ZG) of the adrenal cortex regulates blood pressure and electrolyte homeostasis through aldosterone production. In ZG cells, potassium and angiotensin II (Ang II) trigger calcium oscillations that drive aldosterone synthesis. Changes in serum osmolality also modulate aldosterone production in a chloride-dependent fashion, but the involved proteins remain unclear. Because the chloride channel ClC-2 is activated by hypoosmolality, we investigated its role in ZG osmoregulation.MethodsWe used Clcn2 knockout (KO) and wild-type (WT) mice. Explanted adrenal glands were incubated with iso- and hypotonic solutions for measurements of aldosterone. Acute adrenal slices were studied using calcium and chloride sensitive fluorescent dyes. We also investigated ClC-2's systemic importance by inducing a hyponatremic hypoosmolality in mice using desmopressin.ResultsUnder hypoosmolar conditions, WT adrenals upregulated aldosterone production in vitro, an effect that was absent in the KO. WT cells responded to hypoosmolality with increased intracellular calcium levels. This response was abrogated in KO cells. Intracellular chloride levels were higher in ZG cells from KO adrenal slices. This suggests that ClC-2 provides a hypoosmolality-dependent chloride efflux pathway that is missing in the KO. Systemic hypoosmolality in mice induced by desmopressin did not differentially affect blood aldosterone levels.ConclusionClC-2 plays a role in the ZG's response to reduced extracellular osmolality through chloride outflow, which likely causes depolarization, voltage-dependent calcium influx, and aldosterone production. These data advance our understanding of regulators of aldosterone production.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41606697 · DOI · PMC12852535
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 Control of aldosterone secretion: a model for convergence in cellular signaling pathways [5]
- Research article The Biology of Normal Zona Glomerulosa and Aldosterone-Producing Adenoma: Pathological Implications [6]
- Research article Diacylglycerol production, Ca2+ influx, and protein kinase C activation in sustained cellular responses [7]
- Research article Role of calcium and other mediators in aldosterone secretion from the adrenal glomerulosa cells [8]
- Research article Generation and role of calcium signal in adrenal glomerulosa cells [9]
- Research article Sonic hedgehog signaling during adrenal development [10]
References
- Drelon C, Berthon A, Sahut-Barnola I, Mathieu M, Dumontet T, Rodriguez S, et al.. PKA inhibits WNT signalling in adrenal cortex zonation and prevents malignant tumour development. . 2016. PMID 27624192 · DOI · PMC5027289
- Leng S, Pignatti E, Khetani RS, Shah MS, Xu S, Miao J, et al.. β-Catenin and FGFR2 regulate postnatal rosette-based adrenocortical morphogenesis. . 2020. PMID 32245949 · DOI · PMC7125176
- Göppner C, Orozco IJ, Hoegg-Beiler MB, Soria AH, Hübner CA, Fernandes-Rosa FL, et al.. Pathogenesis of hypertension in a mouse model for human CLCN2 related hyperaldosteronism. . 2019. PMID 31615979 · DOI · PMC6794291
- Volkert M, Dinh HA, Scholl UI, Stölting G. ClC-2 Contributes to Hypotonicity-Induced Adrenal Aldosterone Secretion. . 2026. PMID 41606697 · DOI · PMC12852535
- Spät A, Hunyady L. Control of aldosterone secretion: a model for convergence in cellular signaling pathways. Physiol Rev. 2004. PMID 15044681 · DOI
- Seccia TM, Caroccia B, Gomez-Sanchez EP, Gomez-Sanchez CE, Rossi GP. The Biology of Normal Zona Glomerulosa and Aldosterone-Producing Adenoma: Pathological Implications. Endocr Rev. 2018. PMID 30007283 · DOI · PMC6236434
- Rasmussen H, Isales CM, Calle R, Throckmorton D, Anderson M, Gasalla-Herraiz J, et al.. Diacylglycerol production, Ca2+ influx, and protein kinase C activation in sustained cellular responses. Endocr Rev. 1995. PMID 8529575 · DOI
- Ganguly A, Davis JS. Role of calcium and other mediators in aldosterone secretion from the adrenal glomerulosa cells. Pharmacol Rev. 1994. PMID 7899472 · DOI
- Spät A, Enyedi P, Hajnóczky G, Hunyady L. Generation and role of calcium signal in adrenal glomerulosa cells. Exp Physiol. 1991. PMID 1662965 · DOI
- Laufer E, Kesper D, Vortkamp A, King P. Sonic hedgehog signaling during adrenal development. Mol Cell Endocrinol. 2012. PMID 22020162 · DOI · PMC3288303
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.