ReviewFrontiers in immunology2021
Inflammasome-Dependent Coagulation Activation in Sepsis.
Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 83 citations in OpenAlex.
- Peli1 promotes sepsis-induced inflammation and coagulopathy by maintaining lipg stability in macrophages.Journal of thrombosis and thrombolysis · 2026Article
- Unfractionated Heparin and Low-Molecular-Weight Heparin in Sepsis: Anti-Inflammatory and Anticoagulant Effects Versus No Anticoagulation-A Propensity Score-Matched Analysis.Journal of clinical laboratory analysis · 2026Article
- Itaconate metabolism in regulated cell death.Molecular and cellular biochemistry · 2026Review
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Sepsis-induced immunothrombosis: from cellular crosstalk to multiple organ dysfunction.Frontiers in immunology · 2026Review
- The immunothrombosis pathway linking pulmonary disease to stroke and neurodegeneration: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Macrophage Hypoxia Signaling Pathways and Their Roles in Sepsis.Journal of inflammation research · 2026Review
- Clinical and PET/CT metabolic imaging characteristics across the evolving spectrum of visceral leishmaniasis and associated hemophagocytic lymphohistiocytosis.Frontiers in immunology · 2026Article
- APIP regulates the priming of canonical NLRP3 and non-canonical Caspase-11/4 inflammasomes by binding to TRAF6.Nature communications · 2025Article
- The Role of Inflammasomes in LPS and Gram-Negative Bacterial Sepsis.Journal of clinical medicine · 2025Review
- Prognostic value of baseline plasma D-dimer levels in sepsis: a prospective cohort study.Practical laboratory medicine · 2025Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- Review
- Disseminated intravascular coagulation.Journal of intensive care · 2025Review
- Article
- Targeting the immuno-inflammatory-microbial network: a key strategy for sepsis treatment.Frontiers in immunology · 2025Review
- The Mechanisms of Sepsis Induced Coagulation Dysfunction and Its Treatment.Journal of inflammation research · 2025Review
- Erbin Regulates Tissue Factors Through Ras/Raf Pathway in Coagulation Disorders in Sepsis.Journal of inflammation research · 2025Article
- Immune aging and infectious diseases.Chinese medical journal · 2024Review
- Inhibiting NINJ1-dependent plasma membrane rupture protects against inflammasome-induced blood coagulation and inflammation.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Sepsis is a potentially life-threatening, pathological condition caused by a dysregulated host response to infection. Pathologically, systemic inflammation can initiate coagulation activation, leading to organ dysfunction, and ultimately to multiple organ failure and septic death. The inflammasomes are cytosolic multiprotein signaling complexes that control the host response to diverse pathogen-associated molecular patterns (PAMPs) from microorganisms as well as damage-associated molecular patterns (DAMPs) from dead or dying host cells. Recent studies highlight that the activation of canonical and non-canonical inflammasomes not only mediate the maturation and secretion of interleukin-1 (IL1) family cytokines, but also trigger the release of coagulation factor III, tissue factor (F3, best known as TF) in activated macrophages and monocytes. These emerging functions of inflammasomes in immunocoagulation are further positively regulated by stimulator of interferon response cGAMP interactor 1 (STING1, also known as STING or TMEM173, a hub of the innate immune signaling network) and high mobility group box 1 (HMGB1, a nuclear DAMP). This mini-review will discuss the regulation and function of inflammasome-dependent coagulation activation in sepsis.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.