ReviewMolecular medicine (Cambridge, Mass.)
Estrogen, NFkappaB, and the heat shock response.
Review in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
49 citing papers in PubMed, 107 citations in OpenAlex.
- Distinct Responses of Estrogen Receptor α and β in Chondrocytes Under Excessive Mechanical Stress.Cartilage · 2026Article
- Exercise volume modulates cardiac protection in a type 2 diabetic rat model: differential effects of high- and low-volume moderate-intensity endurance exercise training on diabetic cardiomyopathy.Cardiovascular diabetology. Endocrinology reports · 2026Article
- The impact of fulvestrant on estrogen receptor-driven chromatin dynamics in breast cancer cells.Epigenetics & chromatin · 2026Article
- The Role and Mechanism of Estrogen in Perimenopausal Depression.Current neuropharmacology · 2026Review
- Parkinson's Spectrum Mechanisms in Pregnancy: Exploring Hypothetical Scenarios for MSA in the Era of ART.International journal of molecular sciences · 2025Review
- Genetic architecture of thermotolerance traits in beef cattle: a novel integration of SNP and breed-of-origin effects.Frontiers in genetics · 2025Article
- Sex differences in the association of long-term exposure to heat stress on kidney function in a large Taiwanese population study.Scientific reports · 2024Article
- Resolution of inflammation in chronic disease via restoration of the heat shock response (HSR).Cell stress & chaperones · 2024Review
- Insight into the Potential Mechanisms of Endocrine Disruption by Dietary Phytoestrogens in the Context of the Etiopathogenesis of Endometriosis.International journal of molecular sciences · 2023Review
- Comparative Studies on the Anti-Inflammatory and Apoptotic Activities of Four Greek Essential Oils: Involvement in the Regulation of NF-κΒ and Steroid Receptor Signaling.Life (Basel, Switzerland) · 2023Article
- An In Vivo Screening Model for Investigation of Pathophysiology of Human Implantation Failure.Biomolecules · 2022Review
- Targeting Heat Shock Proteins in Malignant Brain Tumors: From Basic Research to Clinical Trials.Cancers · 2022Review
- NF-κB Signaling in Tumor Pathways Focusing on Breast and Ovarian Cancer.Oncology reviews · 2022Review
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- Review
- Article
- Are Oxidative Stress and Inflammation Mediators of Bone Loss Due to Estrogen Deficiency? A Review of Current Evidence.Endocrine, metabolic & immune disorders drug targets · 2020Review
- Cardioprotective Effect of Decorin in Type 2 Diabetes.Frontiers in endocrinology · 2020Article
- Fernblock® Upregulates NRF2 Antioxidant Pathway and Protects Keratinocytes from PMOxidative medicine and cellular longevity · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Estrogen has pleiotropic actions, among which are its anti-apoptotic, anti-inflammatory, and vasodilatory effects. Recently, an interaction between 17beta-estradiol (E2) and the transcription factor nuclear factor kappaB (NFkappaB) has been identified. NFkappaB has a central role in the control of genes involved in inflammation, proliferation, and apoptosis. Prolonged activation of NFkappaB is associated with numerous inflammatory pathological conditions. An important facet of E2 is its ability to modulate activity of NFkappaB via both genomic and nongenomic actions. E2 can activate NFkappaB rapidly via nongenomic pathways, increase cellular resistance to injury, and induce expression of the protective class of proteins, heat shock proteins (HSPs). HSPs can bind to many of the pro-apoptotic and pro-inflammatory targets of NFkappaB and, thus, indirectly inhibit many of its deleterious effects. In addition, HSPs can block NFkappaB activation and binding directly. Similarly, genomic E2 signaling can inhibit NFkappaB, but does so through alternative mechanisms. This review focuses on the molecular mechanisms of cross-talk between E2, NFkappaB, and HSPs, and the biological relevance of this cross-talk.
Indexed as
Identifiers
What OpenQuestion holds
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.