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Community Series in Advances in Pathogenesis and Therapies of Gout, volume II is written by Jixin Zhong and published by Frontiers Media SA. It's available with International Standard Book Number or ISBN identification 2832560067 (ISBN 10) and 9782832560068 (ISBN 13).
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.