Broken Barriers: A New Take on Sepsis Pathogenesis
Abstract
Recent data indicate that disruption of the microvascular endothelial barrier is a key determinant of the pathogenesis of sepsis.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
A burst in the generation of proinflammatory agents contributes to endothelial barrier breakdown in sepsis, ARDS, dengue fever, and malaria, promoting shock and multiorgan failure in patients.
“A burst in the generation of proinflammatory agents, as a part of an overwhelmed host response, contributes to endothelial barrier breakdown in these diseases, promoting shock and multiorgan failure in patients (1, 2).”
From Targeting β1-integrin inhibits vascular leakage in endotoxemia (2018) · cites this paper as [2]
Increased capillary leakage leading to hypovolemic shock and multiorgan failure is a key event in the pathobiology of several difficult-to-treat conditions, such as sepsis.
“Increased capillary leakage leading to hypovolemic shock and multiorgan failure is a key event in the pathobiology of several difficult-to-treat conditions, such as sepsis (2, 3, 6).”
From Targeting β1-integrin inhibits vascular leakage in endotoxemia (2018) · cites this paper as [2]
The citation lists haven’t been fetched yet
References 46 · Cited by 324
- Authors
- Goldenberg, N. M., Steinberg, B. E., Slutsky, A. S., & Lee, W. L.
- Affiliations
- St. Michael's Hospital (CA)
- University of Toronto (CA)
- Corresponding author
- Lee, Warren L.
- Venue
- Science Translational Medicine
- Published
- 2011-06-22
- Volume
- 3
- Issue
- 88
- Pages
- 88ps25-88ps25
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- OpenAlex
- W2115339089
- Cited by
- 324
- References
- 46
- Citations by year
- 2026: 7 · 2025: 10 · 2024: 17 · 2023: 23 · 2022: 20 · 2021: 23 · 2020: 19 · 2019: 22 · 2018: 20 · 2017: 35 · 2016: 24 · 2015: 26 · 2014: 30 · 2013: 23 · 2012: 20
- FWCI
- 18.48
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- sepsis pathogenesis, endothelial barrier function, tissue edema, endothelial junctions, endothelial cytoskeleton, endothelial activation, animal models of sepsis, clinical trial failure
- MeSH terms
- Animals, Clinical Trials as Topic, Cytoskeleton, Disease Models, Animal, Endothelium, Humans, Intercellular Junctions, Sepsis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review