2022
DOI: 10.2147/jir.s371536
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Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner

Abstract: Silica nanoparticles (SiNPs) are one of the most widely used inorganic nanomaterials, and exposure to SiNP has been demonstrated to induce pulmonary inflammation, primarily promoted by the NLRP3-mediated macrophage pyroptosis. However, mechanisms underlying the activation of NLRP3 signaling are complex, and whether cathepsin B (CTSB), an enzyme released by the ruptured lysosome, could trigger NLRP3 assembly is controversial. Methods: To further characterize the role of CTSB in silica-induced pyroptosis, we con… Show more

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Cited by 12 publications
(7 citation statements)
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“…Remarkably, we did not observe the Np internalization in non-phagocytic mucosa epithelial cells. The permeabilization of the lysosomal membrane is one of the most frequently described mechanisms for activating the inflammasome by particles and Np 47, 48 . We used several inhibitors to confirm the role of the different components of the pathway, and we corroborated the participation of cathepsin B as the early activator of the inflammasome 49, 50 .…”
Section: Discussionmentioning
confidence: 99%
“…Remarkably, we did not observe the Np internalization in non-phagocytic mucosa epithelial cells. The permeabilization of the lysosomal membrane is one of the most frequently described mechanisms for activating the inflammasome by particles and Np 47, 48 . We used several inhibitors to confirm the role of the different components of the pathway, and we corroborated the participation of cathepsin B as the early activator of the inflammasome 49, 50 .…”
Section: Discussionmentioning
confidence: 99%
“…The peptides generated by those proteasomal protein substrates were transported to the ER by the antigen presentation complex (TAP). In the MHC class Ⅱ pathway, the cathepsin B (CTSB) protein—which plays the role of a pro-inflammatory molecule through activating NLRP3 inflammasome ( Ma et al, 2022 ), was downregulated after IT steroid treatments with DVV. In addition, the DEPs related to the complement cascade pathway were also downregulated after IT steroid treatment.…”
Section: Discussionmentioning
confidence: 99%
“…And promoting the release of calcium ions can aggravate the injury of mitochondria, and calcium ion-mediated mitochondrial damage could cause the activation of NLRP3 inflammasome ( Murakami et al, 2012 ). Lysosomal damage releases cathepsin B directly binds to the NLRP3 inflammasome and promotes the activation of the NLRP3 inflammasome ( Ma et al, 2022 ). The release of mitochondrial ROS (mt ROS) and mitochondrial DNA (mt DNA) caused by mitochondrial dysfunction is another important cause of NLRP3 inflammasome activation.…”
Section: Nlrp3 Inflammasome Signaling Pathwaymentioning
confidence: 99%