ArticleJournal of leukocyte biology2017
Frontline Science: Multiple cathepsins promote inflammasome-independent, particle-induced cell death during NLRP3-dependent IL-1β activation.
Article in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.
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
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.
- Inflammasomes and their roles in the pathogenesis of viral hepatitis and their related complications: An updated systematic review.Immunology letters · 2019Pooled it
- Systematic Overview of Solid Particles and Their Host Responses.Frontiers in immunology · 2018Pooled it
- Targeting lysosome-dependent cell death in cancer: towards therapeutic strategies.Biomarker research · 2026Review
- A derivative of PD156707 selectively inhibits NLRP3 inflammasome activation by directly binding to NLRP3.Scientific reports · 2026Article
- Phagocytosis: a process that shapes immune responses to engulfed meals.Nature reviews. Immunology · 2026Review
- Organelles and cancer cell pyroptosis: overview and perspectives.Cell death & disease · 2025Review
- It's a Trap!-Potential of Cathepsins in NET Formation.International journal of molecular sciences · 2025Review
- Cathepsin B Levels Correlate with the Severity of Canine Myositis.Biomolecules · 2025Article
- Mitophagy-related regulated cell death: molecular mechanisms and disease implications.Cell death & disease · 2024Review
- In vitro analysis of the expression of inflammasome, antiviral, and immune genes in an Oreochromis niloticus liver cell line following stimulation with bacterial ligands and infection with tilapia lake virus.Archives of virology · 2024Article
- Pathways of MHC I cross-presentation of exogenous antigens.Seminars in immunology · 2023Review
- NAIP/NLRC4 inflammasome participates in macrophage responses toFrontiers in immunology · 2023Article
- Apilimod activates the NLRP3 inflammasome through lysosome-mediated mitochondrial damage.Frontiers in immunology · 2023Article
- Lysosomal cathepsins act in concert with Gasdermin-D during NAIP/NLRC4-dependent IL-1β secretion.Cell death & disease · 2022Article
- Blocking Caspase-1/Gsdmd and Caspase-3/-8/Gsdme pyroptotic pathways rescues silicosis in mice.PLoS genetics · 2022Article
- Review
- Spatial localization of cathepsins: Implications in immune activation and resolution during infections.Frontiers in immunology · 2022Review
- Lysosomal disruption by orthopedic wear particles induces activation of the NLRP3 inflammasome and macrophage cell death by distinct mechanisms.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2021Article
- Nuclear Receptors in the Control of the NLRP3 Inflammasome Pathway.Frontiers in endocrinology · 2021Review
- Targeting NLRP3 Inflammasome in Translational Treatment of Nervous System Diseases: An Update.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Sterile particles cause several chronic, inflammatory diseases, characterized by repeating cycles of particle phagocytosis and inflammatory cell death. Recent studies have proposed that these processes are driven by the NLRP3 inflammasome, a platform activated by phagocytosed particles, which controls both caspase-1-dependent cell death (pyroptosis) and mature IL-1β secretion. After phagocytosis, particles can disrupt lysosomes, and inhibitor studies have suggested that the resulting release of a lysosomal protease-cathepsin B-into the cytosol somehow activates NLRP3. However, using primary murine macrophages, we found that particle-induced cell death occurs independent of NLRP3/caspase-1 and depends instead on multiple, redundant cathepsins. In contrast, nigericin, a soluble activator of NLRP3 inflammasomes, induced cell death that was dependent on the NLRP3. Interestingly, nigericin-induced cell death depended partly on a single cathepsin, cathepsin X. By inhibiting or silencing multiple cathepsins in macrophages, several key proinflammatory events induced by sterile particles are blocked, including cell death, pro-IL-1β production, and IL-1β secretion. These data suggest that cathepsins might be potential therapeutic targets in particulate-mediated inflammatory disease. In support of this concept, we find that a broad-spectrum cathepsin inhibitor can suppress particle-induced IL-1-dependent peritonitis.
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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 OpenQuestion graph.