ArticleAging and disease2020
Age-induced NLRP3 Inflammasome Over-activation Increases Lethality of SARS-CoV-2 Pneumonia in Elderly Patients.
Article in Aging and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.
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Who cites it
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.
- Coronavirus disease 2019 and neurodegenerative disease: what will the future bring?Current opinion in psychiatry · 2021Pooled it
- COVID-19 Pathophysiology Predicts That Ischemic Stroke Occurrence Is an Expectation, Not an Exception-A Systematic Review.Frontiers in neurology · 2020Pooled it
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Lappaconitine hydrobromide prevents NLRP3-GSDMD-mediated pyroptosis to alleviate sepsis-induced acute lung injury by enhancing NR1H3.Journal of pharmaceutical analysis · 2026Article
- Targeting immunosenescence in lung diseases: mechanistic insights and clinical interventions.BMC medicine · 2026Review
- Age-related increase of NLRC4 inflammasome and TGF-β1 signaling exacerbates airway inflammation and remodeling in asthma.GeroScience · 2026Article
- Identification of immune-mediated aging genes associated with cervical spondylosis through single-cell eQTL Mendelian randomization.Frontiers in immunology · 2026Article
- Human Alveolar Macrophages Detect SARS-CoV-2 Envelope Protein Through TLR2 and TLR4 and Secrete Cytokines in Response.Immunology · 2025Article
- Taletrectinib promotes pyroptosis in colorectal carcinoma via SRC/AKT/mTOR axis inhibition.Scientific reports · 2025Article
- Predicting coronavirus disease 2019 severity using explainable artificial intelligence techniques.Scientific reports · 2025Article
- Otilonium bromide ameliorates pulmonary fibrosis in mice through activating phosphatase PPM1A.Acta pharmacologica Sinica · 2025Article
- Cross-talk between aging resilience pathways and autoimmunity onset.Frontiers in immunology · 2025Review
- Recent advances in COVID-19-induced liver injury: causes, diagnosis, and management.Inflammopharmacology · 2024Review
- Investigating the relationship between lymphocyte cells apoptosis and DNA damage and oxidative stress and therapeutic and clinical outcomes of COVID-19 elderly patients.BMC infectious diseases · 2024Article
- The Interplay of HIV and Long COVID in Sub-Saharan Africa: Mechanisms of Endothelial Dysfunction.Current cardiology reports · 2024Review
- Safety and feasibility of third-party cytotoxic T lymphocytes for high-risk patients with COVID-19.Blood advances · 2024Article
- Sepsis in elderly patients: the role of neutrophils in pathophysiology and therapy.Internal and emergency medicine · 2024Review
- Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration.Molecular neurodegeneration · 2024Review
- Inflammation, Autoimmunity and Neurodegenerative Diseases, Therapeutics and Beyond.Current neuropharmacology · 2024Article
- Evaluation of the relationship between serum interleukin-1β levels and expression of inflammasome-related genes in patients with COVID-19.BMC immunology · 2023Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age is one of the most important prognostic factors associated to lethality in SARS-CoV-2 infection. In multivariate analysis, advanced age was an independent risk factor for death. Recent studies suggest a role for the nucleotide-binding domain and leucine rich repeat containing family, pyrin domain containing 3 (NLRP3) inflammasome activation in lung inflammation and fibrosis in SARS-CoV and SARS-CoV-2 infections. Increased NLRP3/ apoptosis-associated speck-like protein (ASC) mRNA expression and increased caspase-1 activity, have been observed in aged lung, provoking increased and heightened expression levels of mature Interleukin (IL)-1β and IL-18 in aged individuals. Aged individuals have a basal predisposition to over-react to infection, displaying an increased hyper-inflammatory cascade, that seems not to be fully physiologically controlled. NLRP3 inflammasome is over-activated in aged individuals, through deficient mitochondrial functioning, increased mitochondrial Reactive Oxigen Species (mtROS) and/or mitochondrial (mt)DNA, leading to a hyper-response of classically activated macrophages and subsequent increases in IL-1 β. This NLRP3 over-activated status in elderly individuals, is also observed in telomere dysfunctional mice models. In our opinion, the NLRP3 inflammasome plays a central role in the increased lethality observed in elderly patients infected by COVID-19. Strategies blocking inflammasome would deserve to be studied.
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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.