ReviewAntioxidants & redox signaling2014
The mechanisms and physiological relevance of glycocalyx degradation in hepatic ischemia/reperfusion injury.
Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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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
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.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- The Effect of Hypothermic Machine Perfusion to Ameliorate Ischemia-Reperfusion Injury in Donor Organs.Frontiers in immunology · 2022Pooled it
- Graft glycocalyx degradation in human liver transplantation.PloS one · 2019Trial
- Metabolic changes after hepatectomy: Implications for perioperative management and long-term outcomes.World journal of gastrointestinal pathophysiology · 2025Article
- The Role of Machine Perfusion for Liver Transplantation in Children.Pediatric transplantation · 2025Review
- Endothelial Glycocalyx Shedding and Hemodynamic Variables During Hepatic and Pancreatic Resection Surgery.Medicina (Kaunas, Lithuania) · 2025Article
- Rhamnan Sulfate from the SeaweedMarine drugs · 2025Article
- Unraveling the microbial diversity of bovine liver abscesses: isolation, identification, and genomic characterization of theMicrobiology spectrum · 2025Article
- Mechanism of Reactive Oxygen/Nitrogen Species in Liver Ischemia-Reperfusion Injury and Preventive Effect of Chinese Medicine.Chinese journal of integrative medicine · 2025Review
- Factor H-related 1 and heparan sulfate architecture contribute to complement dysregulation in C3 glomerulopathy.Frontiers in immunology · 2025Article
- Review
- Circulating glycocalyx shedding products as biomarkers for evaluating prognosis of patients with out-of-hospital cardiac arrest after return of spontaneous circulation.Scientific reports · 2024Article
- Review
- Pediatric sepsis inflammatory blood biomarkers that correlate with clinical variables and severity of illness scores.Journal of inflammation (London, England) · 2024Article
- Factors influencing glycocalyx degradation: a narrative review.Frontiers in immunology · 2024Review
- Unraveling neurovascular mysteries: the role of endothelial glycocalyx dysfunction in Alzheimer's disease pathogenesis.Frontiers in physiology · 2024Review
- Using Postoperative Coagulation Parameters Within 24 h After Liver Transplantation to Predict Incidence of Stage 3 Acute Kidney Injury (AKI).Annals of transplantation · 2022Article
- Need for a Paradigm Shift in the Treatment of Ischemic Stroke: The Blood-Brain Barrier.International journal of molecular sciences · 2022Review
- Experimental Conditions That Influence the Utility of 2'7'-Dichlorodihydrofluorescein Diacetate (DCFHAntioxidants (Basel, Switzerland) · 2022Article
- Liver Graft Hypothermic Static and Oxygenated Perfusion (HOPE) Strategies: A Mitochondrial Crossroads.International journal of molecular sciences · 2022Review
- Anti-Inflammatory Activity of Orally AdministeredMarine drugs · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
significanceHepatic ischemia/reperfusion (I/R) injury is an inevitable side effect of major liver surgery that can culminate in liver failure. The bulk of I/R-induced liver injury results from an overproduction of reactive oxygen and nitrogen species (ROS/RNS), which inflict both parenchymal and microcirculatory damage. A structure that is particularly prone to oxidative attack and modification is the glycocalyx (GCX), a meshwork of proteoglycans and glycosaminoglycans (GAGs) that covers the lumenal endothelial surface and safeguards microvascular homeostasis. ROS/RNS-mediated degradation of the GCX may exacerbate I/R injury by, for example, inducing vasoconstriction, facilitating leukocyte adherence, and directly activating innate immune cells. RECENT ADVANCES: Preliminary experiments revealed that hepatic sinusoids contain a functional GCX that is damaged during murine hepatic I/R and major liver surgery in patients. There are three ROS that mediate GCX degradation: hydroxyl radicals, carbonate radical anions, and hypochlorous acid (HOCl). HOCl converts GAGs in the GCX to GAG chloramides that become site-specific targets for oxidizing and reducing species and are more efficiently fragmented than the parent molecules. In addition to ROS/RNS, the GAG-degrading enzyme heparanase acts at the endothelial surface to shed the GCX. CRITICAL ISSUES: The GCX seems to be degraded during major liver surgery, but the underlying cause remains ill-defined. FUTURE DIRECTIONS: The relative contribution of the different ROS and RNS intermediates to GCX degradation in vivo, the immunogenic potential of the shed GCX fragments, and the role of heparanase in liver I/R injury all warrant further investigation.
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