ArticlePharmaceuticals (Basel, Switzerland)2023
Neural-Cardiac Inflammasome Axis after Traumatic Brain Injury.
Article in Pharmaceuticals (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Article
- Hemodynamic characterization of cardiac dysfunction after traumatic brain injury using a controlled cortical impact model in male rats.Physiological reports · 2026Article
- Molecular pathways linking traumatic brain injury to cardiovascular dysfunction: therapeutic potential of physical exercise.Metabolic brain disease · 2026Review
- Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles.Journal of extracellular vesicles · 2026Article
- Inflammasomes in glioblastoma.Journal of neuroinflammation · 2026Review
- Association of serum inflammasome proteins and pediatric traumatic brain injury severity.Pediatric research · 2026Article
- NF-Frontiers in cardiovascular medicine · 2026Article
- Bidirectional Interplay Between Traumatic Brain Injury and Cardiovascular Dysfunction in Athletes.Journal of clinical medicine · 2025Review
- Stool-derived extracellular vesicles increase inflammasome signaling and regulate the gut-brain axis after stroke in Alzheimer's disease transgenic mice.Experimental neurology · 2025Article
- Gasdermin-D Genetic Knockout Reduces Inflammasome-Induced Disruption of the Gut-Brain Axis After Traumatic Brain Injury.International journal of molecular sciences · 2025Article
- Immune Response in Traumatic Brain Injury.Current neurology and neuroscience reports · 2024Review
- Development and validation of a machine learning-based model to assess probability of systemic inflammatory response syndrome in patients with severe multiple traumas.BMC medical informatics and decision making · 2024Observational
- Article
- Extracellular vesicles mediate inflammasome signaling in the brain and heart of Alzheimer's disease mice.Frontiers in molecular neuroscience · 2024Article
- Nrf2 functions as a pyroptosis-related mediator in traumatic brain injury and is correlated with cytokines and disease severity: a bioinformatics analysis and retrospective clinical study.Frontiers in neurology · 2024Article
- Development and internal-external validation of a risk prediction nomogram for secondary myocardial injury in traumatic brain injury.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Traumatic brain injury (TBI) affects not only the brain but also peripheral organs like the heart and the lungs, which influences long-term outcomes. A heightened systemic inflammatory response is often induced after TBI, but the underlying pathomechanisms that contribute to co-morbidities remain poorly understood. Here, we investigated whether extracellular vehicles (EVs) containing inflammasome proteins are released after severe controlled cortical impact (CCI) in C57BL/6 mice and cause activation of inflammasomes in the heart that result in tissue damage. The atrium of injured mice at 3 days after TBI showed a significant increase in the levels of the inflammasome proteins AIM2, ASC, caspases-1, -8 and -11, whereas IL-1β was increased in the ventricles. Additionally, the injured cortex showed a significant increase in IL-1β, ASC, caspases-1, -8 and -11 and pyrin at 3 days after injury when compared to the sham. Serum-derived extracellular vesicles (EVs) from injured patients were characterized with nanoparticle tracking analysis and Ella Simple Plex and showed elevated levels of the inflammasome proteins caspase-1, ASC and IL-18. Mass spectrometry of serum-derived EVs from mice after TBI revealed a variety of complement- and cardiovascular-related signaling proteins. Moreover, adoptive transfer of serum-derived EVs from TBI patients resulted in inflammasome activation in cardiac cells in culture. Thus, TBI elicits inflammasome activation, primarily in the atrium, that is mediated, in part, by EVs that contain inflammasome- and complement-related signaling proteins that are released into serum and contribute to peripheral organ systemic inflammation, which increases inflammasome activation in the heart.
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.