Endothelial estrogen receptor alpha (ESR1) regulates cerebral cavernous malformation pathogenesis via MEKK3-KLF signaling pathway.
Overview
- Faculty of Science, School of Life Sciences, Centre for Inflammation, Centenary Institute and University of Technology Sydney (UTS), Sydney NSW, Australia
- School of Medicine, Nanjing University of Chinese Medicine, Nanjing, China
- Sydney Microscopy & Microanalysis, The University of Sydney, Camperdown, NSW, Australia
- NICM Health Research Institute, Western Sydney University, Westmead, NSW, Australia
- Curtin Medical School, Curtin Medical Research Institute, Curtin University, Bentley, WA, Australia
- Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, China
- School of Biomedical Sciences, UNSW Sydney, Kensington, NSW, Australia
Abstract
Cerebral cavernous malformations (CCMs) are common brain hemangioma that can occur sporadically or be inherited. CCM is one of the major causes of hemorrhagic stroke and neurological deficits in children. There are no pharmacological treatments for CCM. Clinical observations suggest that estrogen may have important roles in CCM, however, it has not been investigated. Hence, we investigated the role of estrogen and its nuclear receptors estrogen receptor-α (Esr1) in experimental CCM. To determine the role of endothelial ESR1 in CCM, we crossed homozygous endothelial Esr1 (Esr1fl/
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- geo:GSE137596, at NCBI GEO; found in the text, “CCM patient RNA-seq data analysis”
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, pages, dates, 9 authors, 5 keywords, 4 funders, 39 references.
Cite
This paper
Sadegh, H., Chen, L., Yu, S., Idrees, S., Foley, M., Paudel, K. R., Li, J., Zhao, Y., & Choi, J. P. (2026). Endothelial estrogen receptor alpha (ESR1) regulates cerebral cavernous malformation pathogenesis via MEKK3-KLF signaling pathway. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 0271678X261468891. https://
BibTeX
@article{sadegh2026endot
author = {Sadegh, Hamidreza and Chen, Liwenyu and Yu, Suyun and Idrees, Sobia and Foley, Matthew and Paudel, Keshav Raj and Li, Jia and Zhao, Yang and Choi, Jaesung P},
title = {{Endothelial estrogen receptor alpha (ESR1) regulates cerebral cavernous malformation pathogenesis via MEKK3-KLF signaling pathway}},
journal = {Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism},
year = {2026},
month = jul,
pages = {0271678X261468891},
publisher = {SAGE Publications},
issn = {0271-678X},
doi = {10.1177/
url = {https://
pmid = {42410678},
pmcid = {PMC13388494}
}
RIS
TY - JOUR
AU - Sadegh, Hamidreza
AU - Chen, Liwenyu
AU - Yu, Suyun
AU - Idrees, Sobia
AU - Foley, Matthew
AU - Paudel, Keshav Raj
AU - Li, Jia
AU - Zhao, Yang
AU - Choi, Jaesung P
TI - Endothelial estrogen receptor alpha (ESR1) regulates cerebral cavernous malformation pathogenesis via MEKK3-KLF signaling pathway
T2 - Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
J2 - J Cereb Blood Flow Metab
PY - 2026
DA - 2026/
SP - 0271678X261468891
SN - 0271-678X
PB - SAGE Publications
DO - 10.1177/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1177/
"type": "article-journal",
"title": "Endothelial estrogen receptor alpha (ESR1) regulates cerebral cavernous malformation pathogenesis via MEKK3-KLF signaling pathway",
"container-title": "Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism",
"author": [
{
"family": "Sadegh",
"given": "Hamidreza"
},
{
"family": "Chen",
"given": "Liwenyu"
},
{
"family": "Yu",
"given": "Suyun"
},
{
"family": "Idrees",
"given": "Sobia"
},
{
"family": "Foley",
"given": "Matthew"
},
{
"family": "Paudel",
"given": "Keshav Raj"
},
{
"family": "Li",
"given": "Jia"
},
{
"family": "Zhao",
"given": "Yang"
},
{
"family": "Choi",
"given": "Jaesung P"
}
],
"container-title-short":
"page": "0271678X261468891",
"DOI": "10.1177/
"PMID": "42410678",
"PMCID": "PMC13388494",
"ISSN": "0271-678X",
"publisher": "SAGE Publications",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
7,
6
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1186/s10020-026-01495-4
- Identification of the adhesion GPCR ADGRL4/
ELTD1 as a novel potential prognostic biomarker for cerebral cavernous malformation disease. Journal: Molecular medicine (Cambridge, Mass.)In common: NCBI GEO GSE137596, mouse, 2 references - [2] doi:10.1111/jcmm.71280 [code]
- Rapamycin Partially Reverts Cavernoma Endothelial Cell Phenotype and, When Combined With Lapatinib, Ameliorates Chronic Lesions.Journal: Journal of cellular and molecular medicineIn common: mouse, cellular / molecular, 4 references
- [3] doi:10.1038/s41467-026-71643-1 [code]
- Pericytes are organ-specific regulators of tissue morphogenesis.Journal: Nature communicationsIn common: mouse, cellular / molecular, 2 references
- [4] doi:10.1002/advs.202518421
- Modulation of miR-23b Wnt/
β-catenin Axis Strengthens Endothelial Barrier Properties. Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)In common: stroke, cellular / molecular, 1 reference - [5] doi:10.1073/pnas.2523612123
- A pericyte chloride clamp mechanism governs capillary control of cerebral blood flow.Journal: Proceedings of the National Academy of Sciences of the United States of AmericaIn common: stroke, mouse, cellular / molecular, 1 reference
- [6] doi:10.1523/jneurosci.0019-26.2026 [code]
- Endothelial &
lt;i& gt;Adgrl2& lt;/ i& gt; Expression and Alternative Splicing Controls the Cerebrovasculature. Journal: The Journal of neuroscience : the official journal of the Society for NeuroscienceIn common: stroke, mouse, cellular / molecular, 1 reference - [7] doi:10.1002/alz.71811
- Female vulnerability to microvascular transport dysfunction emerges early across the Alzheimer's disease continuum.Journal: Alzheimer's & dementia : the journal of the Alzheimer's AssociationIn common: stroke, 1 reference
- [8] doi:10.1016/j.nbas.2026.100164
- Single-cell transcriptomic analysis reveals age-related remodeling of brain endothelial cells.Journal: Aging brainIn common: mouse, cellular / molecular, 1 reference
- [9] doi:10.1038/s41467-026-75367-0
- Heterogenous microglial reactivity contrasts with stable vascular transcriptional programs in mouse models of Alzheimer's, CADASIL, and Traumatic Brain Injury.Journal: Nature communicationsIn common: mouse, cellular / molecular, 1 reference
- [10] doi:10.1186/s12974-026-03888-y
- Integrated imaging and molecular profiling reveals APOE4-associated neurovascular and glial disruptions in young adult mice.Journal: Journal of neuroinflammationIn common: mouse, cellular / molecular, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.