ArticleEMBO molecular medicine2024
Liver protects neuron viability and electrocortical activity in post-cardiac arrest brain injury.
Article in EMBO molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
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Who cites it
3 citing papers in PubMed.
- Neuroprognostication After Extracorporeal Cardiopulmonary Resuscitation: ECMO-Specific Challenges and a Multimodal Time-Sensitive Framework.Journal of cardiovascular development and disease · 2026Review
- Animal models of critical illness in the Asia-Pacific region: current practices, shared challenges, and future directions.Intensive care medicine experimental · 2026Review
- [Research progresses in ex vivo liver perfusion technology].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025Review
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Authors and funding
24 authors.
Funding
Abstract
Brain injury is the leading cause of mortality among patients who survive cardiac arrest (CA). Clinical studies have shown that the presence of post-CA hypoxic hepatitis or pre-CA liver disease is associated with increased mortality and inferior neurological recovery. In our in vivo global cerebral ischemia model, we observed a larger infarct area, elevated tissue injury scores, and increased intravascular CD45+ cell adhesion in reperfused brains with simultaneous hepatic ischemia than in those without it. In the ex vivo brain normothermic machine perfusion (NMP) model, we demonstrated that addition of a functioning liver to the brain NMP circuit significantly reduced post-CA brain injury, increased neuronal viability, and improved electrocortical activity. Furthermore, significant alterations were observed in both the transcriptome and metabolome in the presence or absence of hepatic ischemia. Our study highlights the crucial role of the liver in the pathogenesis of post-CA brain injury.
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Registered trials
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