SynthesisInternational journal of molecular sciences2011
Mechanisms of estrogens' dose-dependent neuroprotective and neurodamaging effects in experimental models of cerebral ischemia.
Synthesis in International journal of molecular sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 72 citations in OpenAlex.
- Untargeted Metabolomic Signature of Mice with Ischemic Stroke.Metabolites · 2026Article
- Graptophyllum pictum (Acanthaceae) relieves some hallmarks of endometriosis in an experimental model in Wistar rats.Reproduction & fertility · 2025Article
- Menopausal hormone therapy and dementia: nationwide, nested case-control study.BMJ (Clinical research ed.) · 2023Article
- Involvement of baroreflex deficiency in the age-related loss of estrogen efficacy against cerebral ischemia.Frontiers in aging neuroscience · 2023Article
- Immune regulation based on sex differences in ischemic stroke pathology.Frontiers in immunology · 2023Review
- Tricyclodecan-9-yl-Xanthogenate (D609): Mechanism of Action and Pharmacological Applications.International journal of molecular sciences · 2022Review
- Targeting 17β-estradiol biosynthesis in neural stem cells improves stroke outcome.Frontiers in cellular neuroscience · 2022Article
- Neuroprotective Mechanism of Icariin on Hypoxic Ischemic Brain Damage in Neonatal Mice.Oxidative medicine and cellular longevity · 2022Article
- Sex-Associated Differences in Neurovascular Dysfunction During Ischemic Stroke.Frontiers in molecular neuroscience · 2022Review
- Revealing the Influences of Sex Hormones and Sex Differences in Atrial Fibrillation and Vascular Cognitive Impairment.International journal of molecular sciences · 2021Review
- TGF-β3/Smad3 Contributes to Isoflurane Postconditioning Against Cerebral Ischemia-Reperfusion Injury by Upregulating MEF2C.Cellular and molecular neurobiology · 2020Article
- Natural Drugs as a Treatment Strategy for Cardiovascular Disease through the Regulation of Oxidative Stress.Oxidative medicine and cellular longevity · 2020Review
- Editorial: Steroids and the Brain.Frontiers in endocrinology · 2020Article
- Traumatic Brain Injury-Induced Sex-Dependent Changes in Late-Onset Sensory Hypersensitivity and Glutamate Neurotransmission.Frontiers in neurology · 2020Article
- Age and sex differences in the pathophysiology of acute CNS injury.Neurochemistry international · 2019Review
- The regulatory role of Toll-like receptors after ischemic stroke: neurosteroids as TLR modulators with the focus on TLR2/4.Cellular and molecular life sciences : CMLS · 2019Review
- Disruption of Interneuron Neurogenesis in Premature Newborns and Reversal with Estrogen Treatment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Sex Steroids, Adult Neurogenesis, and Inflammation in CNS Homeostasis, Degeneration, and Repair.Frontiers in endocrinology · 2018Review
- Estrogens as neuroprotectants: Estrogenic actions in the context of cognitive aging and brain injury.Progress in neurobiology · 2017Review
- SIRT1-dependent AMPK pathway in the protection of estrogen against ischemic brain injury.CNS neuroscience & therapeutics · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ever since the hypothesis was put forward that estrogens could protect against cerebral ischemia, numerous studies have investigated the mechanisms of their effects. Despite initial studies showing ameliorating effects, later trials in both humans and animals have yielded contrasting results regarding the fundamental issue of whether estrogens are neuroprotective or neurodamaging. Therefore, investigations of the possible mechanisms of estrogen actions in brain ischemia have been difficult to assess. A recently published systematic review from our laboratory indicates that the dichotomy in experimental rat studies may be caused by the use of insufficiently validated estrogen administration methods resulting in serum hormone concentrations far from those intended, and that physiological estrogen concentrations are neuroprotective while supraphysiological concentrations augment the damage from cerebral ischemia. This evidence offers a new perspective on the mechanisms of estrogens' actions in cerebral ischemia, and also has a direct bearing on the hormone replacement therapy debate. Estrogens affect their target organs by several different pathways and receptors, and the mechanisms proposed for their effects on stroke probably prevail in different concentration ranges. In the current article, previously suggested neuroprotective and neurodamaging mechanisms are reviewed in a hormone concentration perspective in an effort to provide a mechanistic framework for the dose-dependent paradoxical effects of estrogens in stroke. It is concluded that five protective mechanisms, namely decreased apoptosis, growth factor regulation, vascular modulation, indirect antioxidant properties and decreased inflammation, and the proposed damaging mechanism of increased inflammation, are currently supported by experiments performed in optimal biological settings.
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