ArticleJournal of neuroinflammation2020
MCC950, a selective NLPR3 inflammasome inhibitor, improves neurologic function and survival after cardiac arrest and resuscitation.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- NLRP3 Regulation in Neonatal Hypoxic-Ischemic Encephalopathy-Focus on Microglial Activation.International journal of molecular sciences · 2026Article
- Residual Atherothrombotic Risk After Myocardial Infarction: Integrating Lipid, Inflammatory and Thrombotic Pathways.Journal of clinical medicine · 2026Review
- Article
- Skin Application of Inflammasome Inhibitor MCC950 Prevents Psoriasis-like Cutaneous Manifestations and Associated Systemic Inflammation.Inflammation · 2026Article
- Microglial state transitions dominate the brain immune response in the subacute phase after cardiac arrest.Journal of neuroinflammation · 2026Article
- Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review).Molecular medicine reports · 2026Review
- Podocyte-specific acid sphingomyelinase overexpression promotes gasdermin D dependent pyroptosis by impairing autophagic flux during obesity.Frontiers in physiology · 2026Article
- Crosstalk between innate immune signaling pathways and integrated TLR, NLRP3 inflammasome, cGAS-STING, and NF-κB networks in sepsis.Frontiers in cell and developmental biology · 2026Review
- Activation of Intestinal Mast Cells Contributes to Gut Damage After Cardiac Arrest in Mice.Shock (Augusta, Ga.) · 2026Article
- TGF-β1 Improves Nerve Regeneration and Functional Recovery After Sciatic Nerve Injury by Alleviating Inflammation.Biomedicines · 2025Article
- Therapeutic Potential of Gasdermin D-Mediated Myocardial Pyroptosis in Ischaemic Heart Disease: Expanding the Paradigm From Bench to Clinical Insights.Journal of cellular and molecular medicine · 2025Review
- Ferroptosis in Alzheimer's disease: molecular mechanisms and advances in therapeutic strategies.Frontiers in neuroscience · 2025Review
- Novel Targets and Strategies Addressing Residual Cardiovascular Risk in Post-acute Coronary Syndromes Patients.Translational medicine @ UniSa · 2024Review
- Single-cell transcriptomics reveal a hyperacute cytokine and immune checkpoint axis after cardiac arrest in patients with poor neurological outcome.Med (New York, N.Y.) · 2023Article
- The Potential of NLRP3 Inflammasome as a Therapeutic Target in Neurological Diseases.Molecular neurobiology · 2023Review
- Mouse Cardiac Arrest Model for Brain Imaging and Brain Physiology Monitoring During Ischemia and Resuscitation.Journal of visualized experiments : JoVE · 2023Article
- Secondary Cardiovascular Prevention after Acute Coronary Syndrome: Emerging Risk Factors and Novel Therapeutic Targets.Journal of clinical medicine · 2023Review
- Macrophage-NLRP3 Activation Promotes Right Ventricle Failure in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2022Article
- Flufenamic acid improves survival and neurologic outcome after successful cardiopulmonary resuscitation in mice.Journal of neuroinflammation · 2022Article
- The protective effect of MiR-27a on the neonatal hypoxic-ischemic encephalopathy by targeting FOXO1 in rats.Translational pediatrics · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundCardiac arrest (CA) is associated with high morbidity and mortality, even after spontaneous circulation is re-established. This dire situation is partly due to post-CA syndrome for which no specific and effective intervention is available. One key component of post-CA syndrome is sterile inflammation, which affects various organs including the brain. A major effector of sterile inflammation is activated NLRP3 inflammasome, which leads to increased release of interleukin (IL)-1β. However, how NLRP3 inflammasome impacts neuroinflammation and neurologic outcome after CA is largely undefined.
methodsMice were subjected to a potassium-based murine CA and cardiopulmonary resuscitation (CPR) model. MCC950 was used to suppress activation of NLRP3 inflammasome after CA/CPR. Levels of protein and mRNA were examined by Western blotting and quantitative PCR, respectively. Immunologic changes were assessed by measuring cytokine expression and immune cell compositions. CA outcomes, including neurologic deficits, bacterial load in the lung, and survival rate, were evaluated.
resultsUsing our CA/CPR model, we found that NLRP3 inflammasome was activated in the post-CA brain, and that pro-inflammatory cytokine levels, including IL-1β, were increased. After treatment with MCC950, a potent and selective NLRP3 inflammasome inhibitor, mice exhibited improved functional recovery and survival rate during the 14-day observational period after CA/CPR. In line with these findings, IL-1β mRNA levels in the post-CA brain were significantly suppressed after MCC950 treatment. Interestingly, we also found that in MCC950- vs. vehicle-treated CA mice, immune homeostasis in the spleen was better preserved and bacterial load in the lung was significantly reduced.
conclusionsOur data demonstrate that activation of NLRP3 inflammasome could be a key event shaping the post-CA immuno- and neuro-pathology, and identify this pathway as a unique and promising therapeutic target to improve outcomes after CA/CPR.
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