ReviewImmunity, inflammation and disease2023
Research progress on the activation mechanism of NLRP3 inflammasome in septic cardiomyopathy.
Review in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 9 citations in OpenAlex.
- miR-454-3p alleviates LPS-induced cardiomyocyte damage by negatively regulating STAT3 in sepsis-induced cardiomyopathy.Internal and emergency medicine · 2026Article
- Quantitative assessment and prognostic value of myocardial work indices in sepsis-induced cardiomyopathy patients with left ventricular systolic dysfunction.Cardiovascular ultrasound · 2026Article
- MCC950-Loaded M12-Liposome Nanoparticles for Targeted Inhibition of NLRP3 Inflammasome in Sepsis-Induced Muscle Atrophy.Journal of cachexia, sarcopenia and muscle · 2026Article
- The P2X7 receptor/NLRP3 inflammasome signaling axis in sepsis: molecular mechanisms, organ-specific pathophysiology, and emerging therapeutic strategies.Purinergic signalling · 2026Review
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- The central role of mitochondrial pathology in sepsis-induced cardiomyopathy: from molecular mechanisms to clinical translation.Frontiers in cardiovascular medicine · 2026Review
- Association between the atherogenic index of plasma and acute kidney injury in sepsis patients.PloS one · 2026Article
- Inflammasomes as Potential Therapeutic Targets to Prevent Chronic Active Viral Myocarditis-Translating Basic Science into Clinical Practice.International journal of molecular sciences · 2025Review
- Demystifying the Role of Neuroinflammatory Mediators as Biomarkers for Diagnosis, Prognosis, and Treatment of Alzheimer's Disease: A Review.ACS pharmacology & translational science · 2024Review
- Oxidative Stress in Sepsis: A Focus on Cardiac Pathology.International journal of molecular sciences · 2024Article
- The Aquaporin 3 Polymorphism (rs17553719) Is Associated with Sepsis Survival and Correlated with IL-33 Secretion.International journal of molecular sciences · 2024Article
- Research progress on the activation mechanism of NLRP3 inflammasome in septic cardiomyopathy.Immunity, inflammation and disease · 2023Review
- Exploring the pathogenesis of sepsis-induced cardiomyopathy: Multilayered mechanisms and clinical responses.Science progressReview
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is an uncontrolled host response to infection, resulting in a clinical syndrome involving multiple organ dysfunctions. Cardiac damage is the most common organ damage in sepsis. Uncontrolled inflammatory response is an important mechanism in the pathogenesis of septic cardiomyopathy (SCM). NLRP3 inflammasome promotes inflammatory response by controlling the activation of caspase-1 and the release of pro-inflammatory cytokines interleukin IL-1β and IL-18. The role of NLRP3 inflammasome has received increasing attention, but its activation mechanism and regulation of inflammation in SCM remain to be investigated.
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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 Socratic graph.