ArticleInflammation2020
Role of the Nucleotide-Binding Domain-Like Receptor Protein 3 Inflammasome in the Endothelial Dysfunction of Early Sepsis.
Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 36 citations in OpenAlex.
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Comorbidities and Inflammation: How Chronic Diseases Prime the Host Response in Sepsis.International journal of molecular sciences · 2026Review
- Bioinformatic Analysis and Experimental Verification Reveal the Protective Role of Baicalein Against LPS-Induced Endothelial Cell Dysfunction.Journal of inflammation research · 2026Article
- NLRP3 inflammasome in acute lung injury: Cumulative evidence for traditional Chinese medicine and natural products.Chinese herbal medicines · 2025Review
- Melatonin Exerts Positive Effects on Sepsis Through Various Beneficial Mechanisms.Drug design, development and therapy · 2025Review
- Role and Mechanism of cGAS-STING Pathway in Cardiovascular System.Reviews in cardiovascular medicine · 2024Review
- Article
- Regorafenib modulation of the angiopoietin/TIE2 axis in a mouse model of sepsis-induced lung injury.Journal of medicine and life · 2023Article
- Pyroptosis and inflammation‑mediated endothelial dysfunction may act as key factors in the development of erectile dysfunction (Review).Molecular medicine reports · 2023Review
- Article
- PCSK9 Promotes Endothelial Dysfunction During Sepsis Via the TLR4/MyD88/NF-κB and NLRP3 Pathways.Inflammation · 2023Article
- Role of the cGAS-STING Pathway in Aging-related Endothelial Dysfunction.Aging and disease · 2022Article
- Recurrent Hypoglycemia Impaired Vascular Function in Advanced T2DM Rats by Inducing Pyroptosis.Oxidative medicine and cellular longevity · 2022Article
- Review
- Protective Effect of Sirtuin 3 on CLP-Induced Endothelial Dysfunction of Early Sepsis by Inhibiting NF-κB and NLRP3 Signaling Pathways.Inflammation · 2021Article
- Effects of different intensities of continuous training on vascular inflammation and oxidative stress in spontaneously hypertensive rats.Journal of cellular and molecular medicine · 2021Article
- Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy.BMC complementary medicine and therapies · 2021Article
- NLRP3 inflammasome in endothelial dysfunction.Cell death & disease · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Endothelial dysfunction is responsible for multiple organ failure and the high mortality rate of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome plays an essential role in the progression of sepsis. However, the role of NLRP3 inflammasome in the endothelial dysfunction of sepsis has not been fully elucidated. In this study, septic mice were induced by cecal ligation and puncture (CLP) operation, and human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS). The 24-h survival rate after CLP was observed. Vasodilation function of the aorta was detected by vascular reactivity experiments. Expression of p-eNOS, eNOS, TLR4, MYD88, p-p65, p65, p-ikbα, ikbα, iNOS, NLRP3, and IL-1β in the aorta and HUVECs were determined by Western blot. Our results suggest that the p-eNOS expression was downregulated, the endothelium-dependent relaxation function was impaired, and TLR4, MYD88, p-p65, p-ikbα, iNOS, NLRP3, and IL-1β expression increased after CLP. The onset of death was 12 h after CLP, and the mortality rate was nearly 50% at 24 h after operation. The decline of p-eNOS, endothelium-dependent vasodilation function, and survival rate significantly improved with NLRP3-specific inhibitor MCC950 intervention or NLRP3 knockout in CLP mice. The decrease of p-eNOS in HUVECs induced by LPS was alleviated when pretreated with MCC950 or interleukin-1 receptor antagonist (IL-1Ra). In summary, our results indicate that activation of the NLRP3 inflammasome contributes to the development of endothelial dysfunction of early sepsis in mice, suggesting its potential role as a therapeutic target for the treatment of sepsis.
Indexed as
Identifiers
What Socratic 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 Socratic graph.