ArticleBlood2010
Age-dependent vulnerability to endotoxemia is associated with reduction of anticoagulant factors activated protein C and thrombomodulin.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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Who cites it
44 citing papers in PubMed, 85 citations in OpenAlex.
- Distinct patterns of endothelial response to endotoxin in aged mice as compared to young mice.GeroScience · 2026Article
- Age-driven shifts in T and NK cell responses amplify inflammation and coagulopathy during viral infection in mice and humans.Frontiers in immunology · 2026Article
- GDF3 promotes adipose tissue macrophage-mediated inflammation via altered chromatin accessibility during aging.Nature aging · 2026Article
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- Imaging quantitative changes in blood-brain barrier permeability using [Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- CD151 Maintains Endolysosomal Protein Quality to Inhibit Vascular Inflammation.Circulation research · 2024Article
- Age-associated accumulation of B cells promotes macrophage inflammation and inhibits lipolysis in adipose tissue during sepsis.Cell reports · 2024Article
- Impact of age on the host response to sepsis in a murine model of fecal-induced peritonitis.Intensive care medicine experimental · 2024Article
- Thrombogenesis-associated genetic determinants as predictors of thromboembolism and prognosis in cervical cancer.Scientific reports · 2023Article
- Association between age and the host response in critically ill patients with sepsis.Critical care (London, England) · 2022Article
- HLJ1 amplifies endotoxin-induced sepsis severity by promoting IL-12 heterodimerization in macrophages.eLife · 2022Article
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- Metformin attenuated sepsis-associated liver injury and inflammatory response in aged mice.Bioengineered · 2022Article
- Visceral fat-specific regulation of plasminogen activator inhibitor-1 in aged septic mice.Journal of cellular physiology · 2022Article
- High-Precision Isotopic Analysis of Cu and FeFrontiers in chemistry · 2022Article
- Divergent Sepsis Pathophysiology in Older Adults.Antioxidants & redox signaling · 2021Review
- Systemic Immune-Inflammation Index (SII) Can Be an Early Indicator for Predicting the Severity of Acute Pancreatitis: A Retrospective Study.International journal of general medicine · 2021Article
- Time-dependent replicative senescence vs. disturbed flow-induced pre-mature aging in atherosclerosis.Redox biology · 2020Review
- SIRT7 deficiency suppresses inflammation, induces EndoMT, and increases vascular permeability in primary pulmonary endothelial cells.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
The protein C (PC) pathway is an important anticoagulant mechanism that prevents thrombosis during the systemic inflammatory response. Thrombomodulin (TM), an endothelial cell membrane receptor, accelerates the conversion of PC to activated protein C (APC), which leads to the down-regulation of thrombin production and fibrin formation. Induction of acute endotoxemia in young and aged mice with a low dose of bacterial endotoxin lipopolysaccharide (LPS, 2.5 mg/kg) caused a high mortality rate in aged (80%) but not young (0%) mice. After injection with this dose of LPS, fibrin formation was significantly elevated only in aged mice, plasma APC levels were increased only in young mice, and TM expression was profoundly depressed in the aged. The increased thrombosis, suppressed APC level, and decreased TM expression were not observed in young mice receiving a higher dose of LPS (20 mg/kg), which resulted in a mortality rate (78%) equivalent to that seen in aged mice with the low-dose LPS. Mutant mice with reduced TM showed significantly less plasma APC and increased fibrin formation compared with wild-type mice after LPS. These results demonstrate that PC pathway activation is suppressed with aging and is partly responsible for age-associated thrombosis and high mortality during endotoxemia.
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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.