ArticleFrontiers in immunology2022
CaMK4 Promotes Acute Lung Injury Through NLRP3 Inflammasome Activation in Type II Alveolar Epithelial Cell.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- A new paradigm: 46 structural cell types function as environment-supporting innate immune cells, with endothelial and vascular smooth muscle cells as key prototypes.iNew medicine · 2026Article
- Calhm6 Governs Macrophage Polarization Through Chp1-Camk4-Creb1 Axis and Ectosomal Delivery in Inflammatory Responses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MitoQ in sepsis-associated acute lung injury: redox pharmacology, mechanistic evidence, and translational perspectives.Frontiers in pharmacology · 2026Review
- NLRP3 inflammasomes at the ARDS-cancer interface: mechanisms and translational hypotheses.Frontiers in immunology · 2026Review
- Advanced nanotherapies for precision treatment of inflammatory lung diseases.Bioactive materials · 2025Review
- NLRP3 inflammasome in acute lung injury: Cumulative evidence for traditional Chinese medicine and natural products.Chinese herbal medicines · 2025Review
- Amprenavir Mitigates Pepsin-Induced Transcriptomic Changes in Normal and Precancerous Esophageal Cells.International journal of molecular sciences · 2025Article
- Idiopathic Pulmonary Fibrosis Caused by Damaged Mitochondria and Imbalanced Protein Homeostasis in Alveolar Epithelial Type II Cell.Advanced biology · 2025Review
- Cinnamaldehyde Alleviates Alveolar Epithelial Cell Injury in ALI by Inhibiting the CaMKII Pathway.Cell biochemistry and biophysics · 2025Article
- Alveolar epithelial cells in bacterial sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Article
- Comprehensive analysis of m6A modification in lipopolysaccharide-induced acute lung injury in mice.Molecular medicine (Cambridge, Mass.) · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Zang Siwei Qingfei Mixture Alleviates Inflammatory Response to Attenuate Acute Lung Injury by the ACE2/NF-κB Signaling Pathway in Mice.Combinatorial chemistry & high throughput screening · 2024Article
- Role of Lipopolysaccharides in the Inflammation and Pyroptosis of Alveolar Epithelial Cells in Acute Lung Injury and Acute Respiratory Distress Syndrome.Journal of inflammation research · 2024Review
- Acute Lung Injury and the NLRP3 Inflammasome.Journal of inflammation research · 2024Review
- Focus on the role of calcium signaling in ferroptosis: a potential therapeutic strategy for sepsis-induced acute lung injury.Frontiers in medicine · 2024Review
- Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Type II alveolar epithelial cell (AEC II), in addition to its roles in maintaining lung homeostasis, takes an active role in inflammatory response during acute lung injury (ALI). Ca Methods: CaMK4 inhibitor KN-93 was used to investigate the effects of CaMK4 on NLRP3 inflammasome activation. The effects of KN-93 on disease development of lipopolysaccharide (LPS)-induced ALI were also evaluated. The role of CaMK4 on NLRP3 inflammasome activation was explored in human AEC II cell line A549 using KN-93 or CaMK4 siRNA. NLRP3 inflammasome activation was measured by histology immunofluorescence and Western blot. IL-1β and IL-18 were measured by ELISA. Results: Phosphorylation of CaMK4 and the expression of NLRP3 and Caspase-1 p20 were increased in the lungs of LPS-induced ALI mice, which was suppressed by KN-93 as measured by Western blot. Further, the activation of NLRP3 inflammasome was detected in AEC II from patients with acute respiratory distress syndrome (ARDS) and LPS-induced ALI mice. Conclusion: CaMK4 controls the activation of NLRP3 inflammasome in AEC II during LPS-induced ALI. CaMK4 inhibition could be a novel therapeutic approach for the treatment of ALI.
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