ArticleScientific reports2025
Endothelial glycocalyx shedding and oxidative stress in neuronal damage after return of spontaneous circulation in cardiac arrest.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- From Adaptive Resilience to Catastrophic Systems Collapse: Endothelial Entropy, Ferroptotic Propagation, and the Maternal Point of No Return in Emergency Peripartum Hysterectomy.International journal of molecular sciences · 2026Review
- Plasma Heparan Sulfate Structural Variation and Phenotypic Heterogeneity in Pediatric Acute Respiratory Distress Syndrome.Research square · 2026Article
- The Role of Endothelial Glycocalyx in the Pathophysiology of Chronic Kidney Disease and Hypertension: From Molecular Mechanisms to Clinical Biomarkers.Life (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Endothelial glycocalyx (eGC) covers the luminal surface of all vessels. Recent evidence has highlighted its pivotal role in maintaining the integrity of the blood-brain barrier (BBB). Return of spontaneous circulation (ROSC) after cardiac arrest (CA) is a main example of global ischemia-reperfusion (I/R) injury. I/R injury can induce eGC shedding and redox imbalance. This study aims to evaluate the interplay between eGC shedding and oxidative stress (OS) in determing neuronal injury and predicting neurological outcomes following CA. Blood and urine samples were obtained from patients who achieved ROSC after CA. Biomarkers of eGC shedding (syndecan-1 [SDC-1], CD44s, hyaluronan [HYAL], and sulfated glycosaminoglycans [GAGs], of endothelial injury (thrombomodulin [TBML]), of OS (malondialdehyde [MDA], total hydroperoxides [H₂O₂], total antioxidant capacity [CAT], reduced glutathione [GSH], superoxide dismutase [SOD]), and inflammatory mediators (IL-6 and TNF-α) were measured. Neuron-specific enolase (NSE) levels were employed as a surrogate marker of neuronal injury. A score ≥ 4 in the modified Rankin Scale (mRS) at 28 days was considered as poor neurological outcome. Seventy-one patients were included. The levels of SDC-1, HYAL, CD44s, TBML, TAC, SOD, H₂O₂, IL-6, and TNF-α were statistically correlated with neuronal injury. Higher levels of SDC-1, HYAL, CD44s, TBML, MDA, and SOD were observed in patients with poor neurological outcomes. Multivariable logistic regression identified SDC-1 > 796 ng/mL (p = 0.02), TBML > 446 pg/mL (p = 0.03), and MDA > 179 nmol/g (p = 0.03), as predictors of unfavorable neurological outcomes. eGC shedding and OS are interrelated key pathophysiological mechanisms contributing to neuronal injury following CA.
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.