ArticleEndocrinology2010
Estrogen receptor-alpha as a drug target candidate for preventing lung inflammation.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 69 citations in OpenAlex.
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- Impact of Sex on Viral Shedding and Symptom Severity During Acute COVID-19.Pathogens & immunity · 2026Article
- Analysis of the effects of perfluorooctane sulfonate on COPD using network toxicology and molecular docking.iScience · 2025Article
- Estrogen-dependent gene regulation: Molecular basis of TIMP-1 as a sex-specific biomarker for acute lung injury.Physiological reports · 2024Article
- Advances and Challenges in Molecular Imaging of Viral Infections.The Journal of infectious diseases · 2023Review
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- The SARS-CoV-2 spike protein binds and modulates estrogen receptors.Science advances · 2022Article
- The SARS-CoV-2 spike protein binds and modulates estrogen receptors.bioRxiv : the preprint server for biology · 2022Article
- Sex and Liver Disease: The Necessity of an Overarching Theory to Explain the Effect of Sex on Nonreproductive Functions.Endocrinology · 2022Review
- Interplay Between the Immune and Endocrine Systems in the Lung: Implications for TB Susceptibility.Frontiers in immunology · 2022Review
- Newer insights into the pathobiological and pharmacological basis of the sex disparity in patients with pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2021Review
- Zearalenone and the Immune Response.Toxins · 2021Review
- Sex-Specific Differences in Resolution of Airway Inflammation inFrontiers in pharmacology · 2021Article
- Sex Differences, Estrogen Metabolism and Signaling in the Development of Pulmonary Arterial Hypertension.Frontiers in cardiovascular medicine · 2021Review
- SARS-CoV-2 and the possible connection to ERs, ACE2, and RAGE: Focus on susceptibility factors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Acute Exposure to Zearalenone Disturbs Intestinal Homeostasis by Modulating the Wnt/β-Catenin Signaling Pathway.Toxins · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Accumulating evidence shows that estrogens are protective factors in inflammatory lung diseases and are involved in the gender-related incidence of these pathologies. The aim of this study was to identify which estrogen receptor (ER), ER-alpha and/or ER beta, mediates hormone antiinflammatory effects in lung and how gender or aging modify this effect. Acute lung inflammation in wild type, ER alpha or ER beta knockout animals was induced by pleural injection of carrageenan; female mice were used and sham operated, ovariectomized, or ovariectomized and treated with 17beta-estradiol (E(2)) before carrageenan. Our data show that ER alpha, and not ER beta, mediates E(2)-induced reduction of the inflammatory response. By real-time PCR and immunohistochemistry assays, we demonstrate ER alpha expression in the resident and infiltrated inflammatory cells of the lung, in which ER beta could not be detected. In these cells, E(2)-mediated reduction in the expression of inflammatory mediators was also due to ER alpha. In parallel, we observed that female mice were more prone to inflammation as compared with males, suggesting a gender-related difference in lung susceptibility to inflammatory stimuli, whereas the effect of E(2) was similar in the two sexes. Interestingly, aging results in a strong increase in the inflammatory response in both sexes and in the disruption E(2)/ER alpha signaling pathway. In conclusion, our data reveal that E(2) is able to regulate lung inflammation in a gender-unrelated, age-restricted manner. The specific involvement of ER alpha in hormone action opens new ways to identify drug targets that limit the inflammatory component of lung pathologies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.