ReviewFrontiers in endocrinology2020
Estrogen Formation and Inactivation Following TBI: What we Know and Where we Could go.
Review in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 34 citations in OpenAlex.
- Sex and Gender Differences in Physical Activity, Sedentary Behavior, and Sleep During Traumatic Brain Injury Recovery: A Narrative Review.European journal of sport science · 2026Review
- Article
- Sex hormone dysregulation after traumatic brain injury: interactions with sleep disturbances and seizure susceptibility.Frontiers in neuroscience · 2026Review
- Sexual Dysfunction in Traumatic Brain Injury: A Narrative Review and Call for Multidisciplinary Framework.Life (Basel, Switzerland) · 2025Review
- The Influence of Menstrual Cycle Phases on Postconcussion Outcomes and Symptom Reporting: A Scoping Review.Scandinavian journal of medicine & science in sports · 2025Article
- Impacts of traumatic brain injury severity and sex on sleep architecture, duration, and fragmentation.Neurobiology of sleep and circadian rhythms · 2025Article
- Endoscopic Surgery for Deeply Located Intracranial Cysts: Risk Factors for Re-Operation and Symptom Improvement.Yonsei medical journal · 2025Article
- Adipose tissue may not be a major player in the inflammatory pathogenesis of Autism Spectrum Disorder.Brain, behavior, & immunity - health · 2025Article
- Article
- Article
- CCL5 is essential for axonogenesis and neuronal restoration after brain injury.Journal of biomedical science · 2024Article
- Neuroprotection or Sex Bias: A Protective Response to Traumatic Brain Injury in the Females.CNS & neurological disorders drug targets · 2024Review
- Research progress on pleiotropic neuroprotective drugs for traumatic brain injury.Frontiers in pharmacology · 2023Review
- Endometrial proteomic profile of patients with repeated implantation failure.Frontiers in endocrinology · 2023Article
- Editorial: Recent Progress and Perspectives in Neurosteroid Research.Frontiers in endocrinology · 2022Article
- Exploring Sex-Related Differences in Microglia May Be a Game-Changer in Precision Medicine.Frontiers in aging neuroscience · 2022Review
- Neurons and glial cells acquire a senescent signature after repeated mild traumatic brain injury in a sex-dependent manner.Frontiers in neuroscience · 2022Article
- Endogenous and Exogenous Estrogen Exposures: How Women's Reproductive Health Can Drive Brain Aging and Inform Alzheimer's Prevention.Frontiers in aging neuroscience · 2022Review
- Glial estradiol synthesis after brain injury.Current opinion in endocrine and metabolic research · 2021Article
- Sex, Genes, and Traumatic Brain Injury (TBI): A Call for a Gender Inclusive Approach to the Study of TBI in the Lab.Frontiers in neuroscience · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) is responsible for various neuronal and cognitive deficits as well as psychosocial dysfunction. Characterized by damage inducing neuroinflammation, this response can cause an acute secondary injury that leads to widespread neurodegeneration and loss of neurological function. Estrogens decrease injury induced neuroinflammation and increase cell survival and neuroprotection and thus are a potential target for use following TBI. While much is known about the role of estrogens as a neuroprotective agent following TBI, less is known regarding their formation and inactivation following damage to the brain. Specifically, very little is known surrounding the majority of enzymes responsible for the production of estrogens. These estrogen metabolizing enzymes (EME) include aromatase, steroid sulfatase (STS), estrogen sulfotransferase (EST/SULT1E1), and some forms of 17β-hydroxysteroid dehydrogenase (HSD17B) and are involved in both the initial conversion and interconversion of estrogens from precursors. This article will review and offer new prospective and ideas on the expression of EMEs following TBI.
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.