ArticleCritical care (London, England)2014
Endothelial dysfunction is a potential contributor to multiple organ failure and mortality in aged mice subjected to septic shock: preclinical studies in a murine model of cecal ligation and puncture.
Article in Critical care (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Revealing the biological mechanism of acupuncture in alleviating excessive inflammatory responses and organ damage in sepsis: a systematic review.Frontiers in immunology · 2023Pooled it
- Distinct patterns of endothelial response to endotoxin in aged mice as compared to young mice.GeroScience · 2026Article
- Advanced Age in Mice Exacerbates Sepsis-Induced Inflammation, Vascular Permeability, and Multi-Organ Dysfunction.Shock (Augusta, Ga.) · 2026Article
- Association ofInternational journal of molecular sciences · 2025Article
- Precision Profiling of Disease Progression in Murine Models of Sepsis and Septic Shock.International journal of molecular sciences · 2025Article
- Integrating bioinformatics and machine learning for comprehensive analysis and validation of diagnostic biomarkers and immune cell infiltration characteristics in pediatric septic shock.Scientific reports · 2025Article
- Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches.GeroScience · 2024Review
- Tiny Guides, Big Impact: Focus on the Opportunities and Challenges of miR-Based Treatments for ARDS.International journal of molecular sciences · 2024Review
- In Vivo Analysis of Tissue S-Nitrosothiols in Pediatric Sepsis.Antioxidants (Basel, Switzerland) · 2024Article
- Exploration of the role of oxidative stress-related genes in LPS-induced acute lung injury via bioinformatics and experimental studies.Scientific reports · 2023Article
- Aging-Associated Augmentation of Gut Microbiome Virulence Capability Drives Sepsis Severity.mBio · 2023Article
- Organotypic heterogeneity in microvascular endothelial cell responses in sepsis-a molecular treasure trove and pharmacological Gordian knot.Frontiers in medicine · 2023Review
- Association between age and the host response in critically ill patients with sepsis.Critical care (London, England) · 2022Article
- Cell penetrating peptides coupled to an endothelial nitric oxide synthase sequence alter endothelial permeability.Tissue barriers · 2022Article
- Pathophysiology of Sepsis and Genesis of Septic Shock: The Critical Role of Mesenchymal Stem Cells (MSCs).International journal of molecular sciences · 2022Review
- SOCS3 limits TNF and endotoxin-induced endothelial dysfunction by blocking a required autocrine interleukin-6 signal in human endothelial cells.American journal of physiology. Cell physiology · 2022Article
- The Dipeptidyl Peptidase-4 Inhibitor Linagliptin Ameliorates Endothelial Inflammation and Microvascular Thrombosis in a Sepsis Mouse Model.International journal of molecular sciences · 2022Article
- Renal microvascular endothelial cell responses in sepsis-induced acute kidney injury.Nature reviews. Nephrology · 2022Review
- Modulation of oxidative and nitrosative stress attenuates microvascular hyperpermeability in ovine model of Pseudomonas aeruginosa sepsis.Scientific reports · 2021Article
- Endothelial SOCS3 maintains homeostasis and promotes survival in endotoxemic mice.JCI insight · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
introductionThe goal of the current study was to investigate the effect of aging on the development of endothelial dysfunction in a murine model of sepsis, and to compare it with the effect of genetic deficiency of the endothelial isoform of nitric oxide synthase (eNOS).
methodsCecal ligation and puncture (CLP) was used to induce sepsis in mice. Survival rates were monitored and plasma indices of organ function were measured. Ex vivo studies included the measurement of vascular function in thoracic aortic rings, assessment of oxidative stress/cellular injury in various organs and the measurement of mitochondrial function in isolated liver mitochondria.
resultseNOS deficiency and aging both exacerbated the mortality of sepsis. Both eNOS-deficient and aged mice exhibited a higher degree of sepsis-associated multiple organ dysfunction syndrome (MODS), infiltration of tissues with mononuclear cells and oxidative stress. A high degree of sepsis-induced vascular oxidative damage and endothelial dysfunction (evidenced by functional assays and multiple plasma markers of endothelial dysfunction) was detected in aortae isolated from both eNOS(-/-) and aged mice. There was a significant worsening of sepsis-induced mitochondrial dysfunction, both in eNOS-deficient mice and in aged mice. Comparison of the surviving and non-surviving groups of animals indicated that the severity of endothelial dysfunction may be a predictor of mortality of mice subjected to CLP-induced sepsis.
conclusionsBased on the studies in eNOS mice, we conclude that the lack of endothelial nitric oxide production, on its own, may be sufficient to markedly exacerbate the severity of septic shock. Aging markedly worsens the degree of endothelial dysfunction in sepsis, yielding a significant worsening of the overall outcome. Thus, endothelial dysfunction may constitute an early predictor and independent contributor to sepsis-associated MODS and mortality in aged mice.
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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.