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 (742 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
Compounds that interact with estrogen receptors in target tissues to bring about the effects similar to those of estradiol. Estrogens stimulate the female reproductive organs, and the development of secondary female sex characteristics. Estrogenic chemicals include natural, synthetic, steroidal, or non-steroidal compounds.
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: Estrogen; Estrogen Receptor Agonists; Agonists, Estrogen Receptor; Receptor Agonists, Estrogen; Estrogenic Agents; Agents, Estrogenic; Estrogenic Compounds; Compounds, Estrogenic.
Where it fits in the MeSH classification
- Broader topics
- Hormones
- Narrower topics
- Estrogens, Non-Steroidal
- See also
- Receptors, Estrogen; Estrogen Receptor Modulators
Related concepts
- Estrogen Receptors
- Estradiol
- Sex Characteristics
Research landscape
PubMed indexes 69,841 records tagged with the MeSH heading “Estrogens” (counts retrieved 2026-10-29). 6,984 of them (10.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 33,733 records.
Reviews account for 12,240 records (17.5%) and meta-analyses for 280. Randomized controlled trials number 1,425 (2.0%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 33,733 |
| 2000-2009 | 15,409 |
| 2010-2019 | 13,715 |
| 2020 onward | 6,984 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 12,240 | 17.5% |
| Meta-analyses | 280 | 0.4% |
| Randomized controlled trials | 1,425 | 2.0% |
Method: PubMed query "Estrogens"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in pharmacology
Drug evidence builds in layers: laboratory pharmacology describes how a compound acts, pharmacokinetic studies describe how the body handles it, and randomized trials test whether it helps and what harms it causes. Post-marketing surveillance and observational studies reveal rarer adverse effects but cannot prove causation. This page is educational and is not a recommendation to start, stop or change any medicine; decisions about treatment belong with a qualified clinician.
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 |
|---|---|---|---|---|
| Targeting estrogen-regulated system xc- promotes ferroptosis and endocrine sensitivity of ER+ breast cancer | 2025 | Research article Design not recorded in structured metadata | 43 | cc by PMID 39833180 · DOI · PMC11756422 |
| The estrobolome: Estrogen-metabolizing pathways of the gut microbiome and their relation to breast cancer | 2025 | Review article Design not recorded in structured metadata | 42 | cc by PMID 40177842 · DOI · PMC12178105 |
| The Impact of Estrogen Deficiency on Liver Metabolism: Implications for Hormone Replacement Therapy | 2025 | Review article Design not recorded in structured metadata | 30 | cc by PMID 40522859 · DOI · PMC12640711 |
| Systemic and local chronic inflammation and hormone disposition promote a tumor-permissive environment for breast cancer in older women | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42509302 · DOI · PMC13472878 |
Targeting estrogen-regulated system xc- promotes ferroptosis and endocrine sensitivity of ER+ breast cancer [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Estrogen receptor positive (ER+) breast cancer accounts for approximately 70% of cases.
- Closing excerpt
- In conclusion, our data reveal that targeting estrogen-regulated SLC7A11 and SLC3A2 enhances ferroptosis in ER+ breast cancer, offering a novel therapeutic option for patients with ER+ breast cancer, particularly those with endocrine resistance.
- 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 (209 words)
Estrogen receptor positive (ER+) breast cancer accounts for approximately 70% of cases. Endocrine therapies targeting estrogen are the first line therapies for ER+ breast cancer. However, resistance to these therapies occurs in about half of patients, leading to decreased survival rates. Inducing ferroptosis is a promising therapeutic strategy for cancer treatment for refractory and malignant cancers including triple-negative breast cancer. Nevertheless, ER+ breast cancer is relatively resistant to ferroptosis inducers. Here, we uncovered that ERα suppressed ferroptosis in ER+ breast cancer. Silencing ERα triggered ferroptosis, which was attenuated by ferroptosis inhibitor Ferrostatin-1, and was enhanced by ferroptosis inducer Erastin. Mechanistically, ERα transcriptionally upregulated the expression of SLC7A11 and SLC3A2, two subunits of the system xc-, which is one key inhibitory regulator of ferroptosis. Overexpression of the exogenous SLC7A11 and SLC3A2 was able to mitigate ferroptosis induced by ERα inhibition. Moreover, SLC7A11 and SLC3A2 levels were elevated in endocrine-resistant breast cancer cells and tumors. Importantly, the system xc- inhibitor Sorafenib or Imidazole ketone erastin effectively inhibited the growth of tamoxifen-resistant breast cells in vitro and in vivo. In conclusion, our data reveal that targeting estrogen-regulated SLC7A11 and SLC3A2 enhances ferroptosis in ER+ breast cancer, offering a novel therapeutic option for patients with ER+ breast cancer, particularly those with endocrine resistance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39833180 · DOI · PMC11756422
The estrobolome: Estrogen-metabolizing pathways of the gut microbiome and their relation to breast cancer [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Increasing evidence links the gut microbiome to carcinogenesis.
- Closing excerpt
- To clarify the estrobolome's role in breast cancer, future research should use advanced sequencing techniques and methods such as metabolomics and transcriptomics, while considering clinical and behavioral factors that may modify estrobolome mechanisms.
- 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 (189 words)
Increasing evidence links the gut microbiome to carcinogenesis. Disruptions in estrogen regulation by the estrobolome-gut microbiota with estrogen-related functions-may promote breast cancer. However, precise information on estrobolome targets and their underlying mechanisms is limited. This review identifies relevant targets for measuring the estrobolome, focusing on enzymes and microbial taxa involved in processing estrogens, precursors, metabolites, and phytoestrogens, to facilitate the exploration of potential links to breast cancer. Evidence from breast cancer case-control studies is synthesized to assess alignment with these targets, highlight gaps in the evidence, and suggest new paths forward. Findings from case-control studies were heterogeneous and showed limited alignment with estrobolome targets, with only Escherichia coli and Roseburia inulinivorans identified as differentially abundant and functionally relevant between cases and controls. The lack of compelling evidence for estrobolome-specific mechanisms may reflect measurement challenges or may suggest that broader ecological changes in the microbiome, which influence a network of interacting mechanisms, are more influential for carcinogenesis. To clarify the estrobolome's role in breast cancer, future research should use advanced sequencing techniques and methods such as metabolomics and transcriptomics, while considering clinical and behavioral factors that may modify estrobolome mechanisms.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40177842 · DOI · PMC12178105
The Impact of Estrogen Deficiency on Liver Metabolism: Implications for Hormone Replacement Therapy [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Metabolic dysfunction-associated steatotic liver disease (MASLD; previously nonalcoholic fatty liver disease) is the most common chronic liver condition globally.
- Closing excerpt
- In this review, we discuss the burden of MASLD in women, the effect of estrogen deficiency on the processes that drive MASLD development and progression, and the potential sex-specific therapeutic strategies that may prevent or limit MASLD development after menopause.
- 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 (188 words)
Metabolic dysfunction-associated steatotic liver disease (MASLD; previously nonalcoholic fatty liver disease) is the most common chronic liver condition globally. It affects 1 in 3 individuals and is associated with increased liver and cardiovascular mortality. MASLD is a sexually dimorphic condition, and in women the prevalence and severity of MASLD rises significantly following menopause. Preclinical data shows that lack of estrogen promotes multisystem metabolic dysfunction that is characteristic of MASLD. This not only includes hepatic lipid accumulation, insulin resistance, and fibrosis but also extra-hepatic metabolic processes in adipose and skeletal muscle. There are currently no available MASLD treatments tailored to women. The uptake of estrogen-based menopausal hormone replacement therapy (HRT) has seen a dramatic increase in recent years. Despite the changing attitudes toward HRT and the strong evidence base implicating estrogen deficiency in the development of MASLD, the impact of HRT on MASLD in postmenopausal women is poorly studied. In this review, we discuss the burden of MASLD in women, the effect of estrogen deficiency on the processes that drive MASLD development and progression, and the potential sex-specific therapeutic strategies that may prevent or limit MASLD development after menopause.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40522859 · DOI · PMC12640711
Systemic and local chronic inflammation and hormone disposition promote a tumor-permissive environment for breast cancer in older women [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Estrogen receptor-positive (ER+) breast cancer is the most common subtype of breast cancer and is an age-related disease.
- Closing excerpt
- These findings support a model linking age-associated hormonal and inflammatory changes to features of a tumor-permissive microenvironment in ER+ breast cancer.
- 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 (156 words)
Estrogen receptor-positive (ER+) breast cancer is the most common subtype of breast cancer and is an age-related disease. How systemic and tumor microenvironment hormone signaling intersects with chronic inflammation and how this shapes aging-associated tumor biology remain incompletely understood. Here, using an aged rat model of ER+ tumors, we identify age-associated differences in tumor development and immune features. In parallel, analysis of samples from patients with ER+/HER2- breast cancer and age-matched controls demonstrated estrone-predominant systemic estrogen patterns and increased tumor HSD17B7 expression in older patients, consistent with enhanced local estrone-to-estradiol conversion. In patient-derived organoids from older women, pharmacologic inhibition of HSD17B7 reduced estrogen conversion and proliferation-associated transcriptional programs. Tumors from older patients also exhibited chemokine enrichment, including CCL2, associated with immunosuppressive macrophage features. Targeting both estrogen signaling and chemokine pathways attenuated macrophage polarization ex vivo. These findings support a model linking age-associated hormonal and inflammatory changes to features of a tumor-permissive microenvironment in ER+ breast cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42509302 · DOI · PMC13472878
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 Type and timing of menopausal hormone therapy and breast cancer risk: individual participant meta-analysis of the worldwide epidemiological evidence [5]
- Research article Hormone replacement therapy and cognition: systematic review and meta-analysis [6]
- Research article The Role of Estrogen in Insulin Resistance: A Review of Clinical and Preclinical Data [7]
- Research article Long-term hormone therapy for perimenopausal and postmenopausal women [8]
- Research article Cycle regimens for frozen-thawed embryo transfer [9]
- Research article Efficacy of phytoestrogens for menopausal symptoms: a meta-analysis and systematic review [10]
References
- Cao J, Zhou T, Wu T, Lin R, Huang J, Shi D, et al.. Targeting estrogen-regulated system xc- promotes ferroptosis and endocrine sensitivity of ER+ breast cancer. . 2025. PMID 39833180 · DOI · PMC11756422
- Larnder AH, Manges AR, Murphy RA. The estrobolome: Estrogen-metabolizing pathways of the gut microbiome and their relation to breast cancer. . 2025. PMID 40177842 · DOI · PMC12178105
- Dong J, Dennis KMJH, Venkatakrishnan R, Hodson L, Tomlinson JW. The Impact of Estrogen Deficiency on Liver Metabolism: Implications for Hormone Replacement Therapy. . 2025. PMID 40522859 · DOI · PMC12640711
- Carleton N, Chang AC, Lee S, Li R, Zou J, Brown DD, et al.. Systemic and local chronic inflammation and hormone disposition promote a tumor-permissive environment for breast cancer in older women. . 2026. PMID 42509302 · DOI · PMC13472878
- Collaborative Group on Hormonal Factors in Breast Cancer. Type and timing of menopausal hormone therapy and breast cancer risk: individual participant meta-analysis of the worldwide epidemiological evidence. Lancet. 2019. PMID 31474332 · DOI · PMC6891893
- LeBlanc ES, Janowsky J, Chan BK, Nelson HD. Hormone replacement therapy and cognition: systematic review and meta-analysis. JAMA. 2001. PMID 11255426 · DOI
- De Paoli M, Zakharia A, Werstuck GH. The Role of Estrogen in Insulin Resistance: A Review of Clinical and Preclinical Data. Am J Pathol. 2021. PMID 34102108 · DOI
- Marjoribanks J, Farquhar C, Roberts H, Lethaby A, Lee J. Long-term hormone therapy for perimenopausal and postmenopausal women. Cochrane Database Syst Rev. 2017. PMID 28093732 · DOI · PMC6465148
- Ghobara T, Gelbaya TA, Ayeleke RO. Cycle regimens for frozen-thawed embryo transfer. Cochrane Database Syst Rev. 2017. PMID 28675921 · DOI · PMC6483463
- Chen MN, Lin CC, Liu CF. Efficacy of phytoestrogens for menopausal symptoms: a meta-analysis and systematic review. Climacteric. 2015. PMID 25263312 · DOI · PMC4389700
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 2026-10-29.
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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.