About this Research Topic
This Research Topic is the second volume of the “Advances in Pathogenesis and Therapies of Gout” Community Series. Please see Volume I here
Gout is one of the most common metabolic disorders in human caused by inflammatory responses to the deposition of monosodium urate (MSU) crystals. The uric acid levels exceed the physiological saturation concentration, which lead to monosodium urate crystal (MSU) formation. The pathogenesis of gout is that MSU crystal triggers strong inflammatory response by activating macrophages in tissues and promoting the collection of neutrophils to tissues or organs. It has been reported that many soluble mediators are implicated in the initiation and amplification of the gout flare, including pro-inflammatory cytokines, lipid mediators and complement. However, the inflammasome and IL-1β has a pivotal role in initiation of the gout flare. Interestingly, The gout flare is a self-limiting inflammation, and several mechanisms of resolution have been proposed, such as neutrophil extracellular traps, negative regulators of inflammasome and TLR signaling, and anti-inflammatory cytokines. It is noteworthy that gout is closely related to many diseases, especially cardiovascular diseases. Cardiovascular risk of gout and hyperuricemia has been well established and is associated with persistent inflammation, thereby promoting cardiovascular damage, increasing incidence rate and mortality.
The goal of this Research Topic is to further our understanding of the inflammatory regulation in the molecular pathophysiology of acute and chronic gout. Understanding the role of inflammation in the development of gout will potentially lead to significant drug options for treatment, particularly since gout was closely associated with many diseases.
We invite authors to contribute Original Research articles as well as Reviews that focus on the topic of inflammatory regulation and clinical management in gout. Potential topics include but are not limited to the following:
• Advances in gout flare pathogenesis, such as new molecular, cellular and microbiota pathways;
• Negative Regulators of inflammasome and TLR Signaling in gout self-resolution;
• Identification and validation of novel agents in the pathogenesis of gout with other organs damage, such as cardiovascular diseases;
• Novel inflammatory-related agents and technologies with potential applications in the diagnosis and treatment of gout.
The Topic Editors declare no competing interests with regard to the Research Topic subject.
Gout is one of the most common metabolic disorders in human caused by inflammatory responses to the deposition of monosodium urate (MSU) crystals. The uric acid levels exceed the physiological saturation concentration, which lead to monosodium urate crystal (MSU) formation. The pathogenesis of gout is that MSU crystal triggers strong inflammatory response by activating macrophages in tissues and promoting the collection of neutrophils to tissues or organs. It has been reported that many soluble mediators are implicated in the initiation and amplification of the gout flare, including pro-inflammatory cytokines, lipid mediators and complement. However, the inflammasome and IL-1β has a pivotal role in initiation of the gout flare. Interestingly, The gout flare is a self-limiting inflammation, and several mechanisms of resolution have been proposed, such as neutrophil extracellular traps, negative regulators of inflammasome and TLR signaling, and anti-inflammatory cytokines. It is noteworthy that gout is closely related to many diseases, especially cardiovascular diseases. Cardiovascular risk of gout and hyperuricemia has been well established and is associated with persistent inflammation, thereby promoting cardiovascular damage, increasing incidence rate and mortality.
The goal of this Research Topic is to further our understanding of the inflammatory regulation in the molecular pathophysiology of acute and chronic gout. Understanding the role of inflammation in the development of gout will potentially lead to significant drug options for treatment, particularly since gout was closely associated with many diseases.
We invite authors to contribute Original Research articles as well as Reviews that focus on the topic of inflammatory regulation and clinical management in gout. Potential topics include but are not limited to the following:
• Advances in gout flare pathogenesis, such as new molecular, cellular and microbiota pathways;
• Negative Regulators of inflammasome and TLR Signaling in gout self-resolution;
• Identification and validation of novel agents in the pathogenesis of gout with other organs damage, such as cardiovascular diseases;
• Novel inflammatory-related agents and technologies with potential applications in the diagnosis and treatment of gout.
The Topic Editors declare no competing interests with regard to the Research Topic subject.
Keywords: Gout, inflammasome, self-solution, hyperuricemia, monosodium urate
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
