The DOI matches its Crossref record; 292 of the 292 references it cites were found in a registry or an index.
The G protein-coupled oestrogen receptor GPER in health and disease: an update
Open accessAbstract
Oestrogens and their receptors contribute broadly to physiology and diseases. In premenopausal women, endogenous oestrogens protect against cardiovascular, metabolic and neurological diseases and are involved in hormone-sensitive cancers such as breast cancer. Oestrogens and oestrogen mimetics mediate their effects via the cytosolic and nuclear receptors oestrogen receptor-α (ERα) and oestrogen receptor-β (ERβ) and membrane subpopulations as well as the 7-transmembrane G protein-coupled oestrogen receptor (GPER). GPER, which dates back more than 450 million years in evolution, mediates both rapid signalling and transcriptional regulation. Oestrogen mimetics (such as phytooestrogens and xenooestrogens including endocrine disruptors) and licensed drugs such as selective oestrogen receptor modulators (SERMs) and downregulators (SERDs) also modulate oestrogen receptor activity in both health and disease. Following up on our previous Review of 2011, we herein summarize the progress made in the field of GPER research over the past decade. We will review molecular, cellular and pharmacological aspects of GPER signalling and function, its contribution to physiology, health and disease, and the potential of GPER to serve as a therapeutic target and prognostic indicator of numerous diseases. We also discuss the first clinical trial evaluating a GPER-selective drug and the opportunity of repurposing licensed drugs for the targeting of GPER in clinical medicine.
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“Both PLCD3 and SLC22A5 are associated with estrogen‐related signaling pathways (Figure S5), with PLCD3 being a phospholipase C (PLC) isozyme activated by G protein‐coupled estrogen receptor (GPER) 60 , 61 and SLC22A5 being a carnitine transport protein transcriptionally regulated by estrogen receptors. 62”
From Unraveling sex differences in Alzheimer's disease and related endophenotypes with brain proteomes (2025) · cites this paper as [61]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Both PLCD3 and SLC22A5 are associated with estrogen‐related signaling pathways (Figure S5), with PLCD3 being a phospholipase C (PLC) isozyme activated by G protein‐coupled estrogen receptor (GPER) 60 , 61 and SLC22A5 being a carnitine transport protein transcriptionally regulated by estrogen receptors. 62”
From Unraveling sex differences in Alzheimer's disease and related endophenotypes with brain proteomes (2025) · cites this paper as [61]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“PLCD3 is a phospholipase C (PLC) isozyme activated by G protein‐coupled estrogen receptor (GPER) and is involved in phosphoinositide turnover and protein kinase C (PKC) activation. 60 , 61”
From Unraveling sex differences in Alzheimer's disease and related endophenotypes with brain proteomes (2025) · cites this paper as [61]
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Hsu, S.-H., Chen, L.-R., & Chen, K.-H. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252212139 · Cited by 105
Identification, structure, and agonist design of an androgen membrane receptor
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Metadata
- Authors
- Prossnitz, E. R., & Barton, M.
- Affiliations
- University of New Mexico (US)
- University of Zurich (CH)
- Corresponding author
- Prossnitz, Eric R.
- Barton, Matthias
- Venue
- Nature Reviews Endocrinology
- Published
- 2023-05-16
- Volume
- 19
- Issue
- 7
- Pages
- 407-424
- ISSN
- 1759-5029 (ISSN-L)
- 1759-5037
- PMC
- PMC10187525
- OpenAlex
- W4376639723
- Cited by
- 231
- References
- 292
- Citations by year
- 2026: 63 · 2025: 91 · 2024: 68 · 2023: 9
- FWCI
- 8.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Reviews Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation
- Dialysis Clinics
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (122504, 108258)
- National Institutes of Health (CA118100, CA163890, GM121176)
- National Cancer Institute (R01CA127731, R01CA163890, P30CA118100, R01CA194496)
- National Institute of General Medical Sciences (P20GM121176)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Keywords
- endocrine disruptors, selective estrogen receptor modulators, estrogen receptor alpha, estrogen receptor beta, therapeutic target, drug repurposing
- MeSH terms
- Breast Neoplasms, Estrogens, Female, Humans, Receptors, Estrogen, GTP-Binding Proteins, Receptors, G-Protein-Coupled, Estrogen Receptor alpha, Estrogen Receptor beta
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