ArticleScientific reports2017
Phagocytosis of environmental or metabolic crystalline particles induces cytotoxicity by triggering necroptosis across a broad range of particle size and shape.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.
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Who cites it
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Results from omic approaches in rat or mouse models exposed to inhaled crystalline silica: a systematic review.Particle and fibre toxicology · 2024Pooled it
- Systematic Overview of Solid Particles and Their Host Responses.Frontiers in immunology · 2018Pooled it
- Apoptosis, ferroptosis, necrosis, necroptosis and pyroptosis in the formation of calcium oxalate kidney stones.Urolithiasis · 2025Review
- Coal dust particles can upregulate the expression of NLRP3 inflammasome components in rat alveolar macrophages through phagocytosis.Scientific reports · 2025Article
- Mechanistic studies of CaScientific reports · 2025Article
- Cell death‑related molecules and targets in the progression of urolithiasis (Review).International journal of molecular medicine · 2024Review
- Article
- Adenine overload induces ferroptosis in human primary proximal tubular epithelial cells.Cell death & disease · 2022Article
- Think Beyond Particle Cytotoxicity: When Self-Cellular Components Released After Immunogenic Cell Death Explain Chronic Disease Development.Frontiers in toxicology · 2022Review
- DNA/RNA heteroduplex oligonucleotide technology for regulating lymphocytes in vivo.Nature communications · 2021Article
- TRPV1 Hyperfunction Contributes to Renal Inflammation in Oxalate Nephropathy.International journal of molecular sciences · 2021Article
- Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity.Frontiers in toxicology · 2021Review
- Alum triggers infiltration of human neutrophils ex vivo and causes lysosomal destabilization and mitochondrial membrane potential-dependent NET-formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Potentially Pathogenic Calcium Oxalate Dihydrate and Titanium Dioxide Crystals in the Alzheimer's Disease Entorhinal Cortex.Journal of Alzheimer's disease : JAD · 2020Article
- Aconitine induces cardiomyocyte damage by mitigating BNIP3-dependent mitophagy and the TNFα-NLRP3 signalling axis.Cell proliferation · 2020Article
- Statins ameliorate cholesterol-induced inflammation and improve AQP2 expression by inhibiting NLRP3 activation in the kidney.Theranostics · 2020Article
- Plasma Proteins and Platelets Modulate Neutrophil Clearance of Malaria-Related Hemozoin Crystals.Cells · 2019Article
- B-RAFCells · 2019Article
- The Pyroptotic Cell Death Effector Gasdermin D Is Activated by Gout-Associated Uric Acid Crystals but Is Dispensable for Cell Death and IL-1β Release.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Cell Death in the Kidney.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In crystallopathies, crystals or crystalline particles of environmental and metabolic origin deposit within tissues, induce inflammation, injury and cell death and eventually lead to organ-failure. The NLRP3-inflammasome is involved in mediating crystalline particles-induced inflammation, but pathways leading to cell death are still unknown. Here, we have used broad range of intrinsic and extrinsic crystal- or crystalline particle-sizes and shapes, e.g. calcium phosphate, silica, titanium dioxide, cholesterol, calcium oxalate, and monosodium urate. As kidney is commonly affected by crystallopathies, we used human and murine renal tubular cells as a model system. We showed that all of the analysed crystalline particles induce caspase-independent cell death. Deficiency of MLKL, siRNA knockdown of RIPK3, or inhibitors of necroptosis signaling e.g. RIPK-1 inhibitor necrostatin-1s, RIPK3 inhibitor dabrafenib, and MLKL inhibitor necrosulfonamide, partially protected tubular cells from crystalline particles cytotoxicity. Furthermore, we identify phagocytosis of crystalline particles as an upstream event in their cytotoxicity since a phagocytosis inhibitor, cytochalasin D, prevented their cytotoxicity. Taken together, our data confirmed the involvement of necroptosis as one of the pathways leading to cell death in crystallopathies. Our data identified RIPK-1, RIPK3, and MLKL as molecular targets to limit tissue injury and organ failure in crystallopathies.
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