ArticleMolecular medicine reports2021
Ulinastatin protects against sepsis‑induced myocardial injury by inhibiting NLRP3 inflammasome activation.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.
- The core role of central nervous system in sepsis-related organ damage.Frontiers in immunology · 2025Pooled it
- The impact of ulinastatin on wound infection and healing in patients with burn wounds: A meta-analysis.International wound journal · 2024Pooled it
- The impact of ulinastatin on lymphocyte apoptosis and autophagy in sepsis patients.Scientific reports · 2024Trial
- Protective role of IRG1/itaconate in acute myocardial injury: association with NLRP3 inflammasome and oxidative stress.Scientific reports · 2026Article
- Recombinant human urinary trypsin inhibitor improves the immunological function of splenic dendritic cells in mice with acute lung injury.European journal of medical research · 2025Article
- Targeting c-Jun orchestrates heat stroke-induced myocardial injury and reveals its biomarker potential.Frontiers in immunology · 2025Article
- Urinary trypsin inhibitor: anti-inflammatory effects in septic mice and molecular insights in bacterial lipoprotein-induced THP-1 cells.Central-European journal of immunology · 2025Article
- Mechanisms and Targeted Therapeutic Strategies in Sepsis-Induced Myocardial Dysfunction: The Role of NLRP3 Inflammasome-Mediated Inflammation.Journal of inflammation research · 2025Review
- Regulation of mitochondrial autophagy by lncRNA MALAT1 in sepsis-induced myocardial injury.European journal of medical research · 2024Article
- Acute exposure to LPS induces cardiac dysfunction via the activation of the NLRP3 inflammasome.Scientific reports · 2024Article
- Ulinastatin modulates NLRP3 inflammasome pathway in PTZ-induced epileptic mice: A potential mechanistic insight.Heliyon · 2024Article
- [Recent research on pyroptosis in sepsis-induced myocardial depression].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Review
- Molecular hydrogen attenuates sepsis-induced cardiomyopathy in mice by promoting autophagy.BMC anesthesiology · 2024Article
- Exploring and Validating the Mechanism of Ulinastatin in the Treatment of Sepsis-Associated Encephalopathy Based on Transcriptome Sequencing.Journal of inflammation research · 2024Article
- The role of TLR4/MyD88/NF-κB in the protective effect of ulinastatin on the intestinal mucosal barrier in mice with sepsis.BMC anesthesiology · 2023Article
- Research progress on the activation mechanism of NLRP3 inflammasome in septic cardiomyopathy.Immunity, inflammation and disease · 2023Review
- Protective effect and mechanism of γ-secretase inhibitor on myocardial injury in sepsis rats.American journal of translational research · 2023Article
- Long Noncoding RNA 00472: A Novel Biomarker in Human Diseases.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial injury is the primary manifestation of multiple organ dysfunction during sepsis, however, the mechanisms underlying sepsis‑induced myocardial injury remain unclear. Similarly, no effective therapeutics have yet been developed for myocardial injury. In the present study, the role of the NOD‑like receptor 3 (NLRP3) inflammasome on cardiac function were characterized and the effects of different ulinastatin (UTI) doses in protecting a septic rat model from myocardial injury were elucidated. To evaluate UTI efficacy on cardiac function, its effects on anti‑inflammatory mediators were analyzed and its cardioprotective effects were investigated. It was demonstrated that circulatory levels of tumor necrosis factor‑α and interleukin‑1β were elevated during sepsis. It was also observed that NLRP3 and caspase‑1 expression enhanced post‑cecal ligation and puncture (CLP), and that high UTI levels protected against myocardial injury induced by sepsis. To the best of our knowledge, this is the first study to demonstrate that the mechanisms underpinning UTI‑mediated myocardial protection were due to the downregulation of the NLRP3/caspase‑1/IL‑1β signaling pathway. Based on these findings, it is proposed that UTI exerts beneficial effects during sepsis‑induced myocardial injury.
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Registered trials
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