Inflammasomes are master regulators belonging to the innate immune system, especially in macrophages, and are key sensors involved in maintaining the integrity in response to cytolytic pathogens (Pathogen-Associated Molecular Patterns) or stress signals (Damage-Associated Molecular Patterns). The most characterized member, the NLRP3 inflammasome, is a cytoplasmic complex that is typically composed of a sensor molecule, such as NOD-like receptors (NLRs), an adaptor protein, including ASC, and an effector protein, such as caspase 1. Upon stimulation, inflammasome complex components associate to promote both the cleavage of the pro-caspase 1 into active caspase-1 and the subsequent release of matured pro-inflammatory cytokines, including IL-18 and IL-1β. The deficiency or overactivation of such an important sensor leads to many diseases. For instance, the accumulation of metabolic waste including urea crystals, hydroxyapatite crystals, and cholesterol crystals is associated with chronic inflammatory diseases such as gouty, rheumatoid arthritis, and atherosclerosis, respectively. Beyond classical activation signals, metabolic pathways such as acetate production and glycolysis have been shown to interact with the NLRP3 inflammasome. As such, NLRP3 deregulation has been suggested to trigger metabolic diseases including atherosclerosis, type 2 diabetes, and non-alcoholic fatty liver disease.
In this Research Topic, we welcome the submission of Original Research, Review, and Mini Review articles on basic, experiment, pre-clinical and clinical research. Submissions may cover but are not limited to the following aims:
-To better understand the mechanism by which inflammasome deregulation triggers metabolic diseases
-To bring together evidence on the mechanisms involved in metabolic disorders and promote inflammasome activation and chronic inflammation
-To review the state of the art in inflammasome-driven metabolic diseases and metabolites-triggered inflammasome impairment
Inflammasomes are master regulators belonging to the innate immune system, especially in macrophages, and are key sensors involved in maintaining the integrity in response to cytolytic pathogens (Pathogen-Associated Molecular Patterns) or stress signals (Damage-Associated Molecular Patterns). The most characterized member, the NLRP3 inflammasome, is a cytoplasmic complex that is typically composed of a sensor molecule, such as NOD-like receptors (NLRs), an adaptor protein, including ASC, and an effector protein, such as caspase 1. Upon stimulation, inflammasome complex components associate to promote both the cleavage of the pro-caspase 1 into active caspase-1 and the subsequent release of matured pro-inflammatory cytokines, including IL-18 and IL-1β. The deficiency or overactivation of such an important sensor leads to many diseases. For instance, the accumulation of metabolic waste including urea crystals, hydroxyapatite crystals, and cholesterol crystals is associated with chronic inflammatory diseases such as gouty, rheumatoid arthritis, and atherosclerosis, respectively. Beyond classical activation signals, metabolic pathways such as acetate production and glycolysis have been shown to interact with the NLRP3 inflammasome. As such, NLRP3 deregulation has been suggested to trigger metabolic diseases including atherosclerosis, type 2 diabetes, and non-alcoholic fatty liver disease.
In this Research Topic, we welcome the submission of Original Research, Review, and Mini Review articles on basic, experiment, pre-clinical and clinical research. Submissions may cover but are not limited to the following aims:
-To better understand the mechanism by which inflammasome deregulation triggers metabolic diseases
-To bring together evidence on the mechanisms involved in metabolic disorders and promote inflammasome activation and chronic inflammation
-To review the state of the art in inflammasome-driven metabolic diseases and metabolites-triggered inflammasome impairment