Description
Title: The Fibrosis-Related NLRP3 Inflammasome Mechanism and Regulation
Abstract: Chronic inflammation frequently leads to fibrosis as a side effect. Extracellular matrix is excessively deposited, which is how it is identified. This causes structural changes in the tissue, which result in long-term harm and organ dysfunction. Fibrosis can pose a serious threat to human life, depending on the organ it affects. The NLRP3 (NOD-, LRR- and pyrin-domain-containing protein 3) inflammasome appears to be important in the pathogenesis of fibrotic disease, despite the fact that the molecular basis of fibrosis is still poorly understood. The inflammatory pathway that has received the most research to date is the NLRP3 inflammasome. It is an essential part of the innate immune system, and when it is activated, IL-1 and IL-18 are secreted. The chronic upregulation of IL-1 and IL-18, as well as the subsequent autocrine signaling that maintains an activated inflammasome, are strongly associated with NLRP3 activation and myofibroblast differentiation. Although IL-1 and IL-18 are both profibrotic, IL-1 also has some antifibrotic properties. NLRP3 reacts to a wide variety of signals, all of which share an unknown unifying trigger. The regulation of the NLRP3 inflammasome has been extensively studied for more than 20 years, but it is still not fully understood. What is understood about NLRP3 is that it is complexly regulated and activated, and that this regulation and activation are not only influenced by different activators but also by numerous post-translational modifications. The search for NLRP3 inhibitors to treat chronic diseases has intensified more recently. Inflammasome NLRP3’s role in fibrotic disorders across a variety of tissues is discussed in this review. It covers various therapeutics that have been created or are currently being developed that directly target NLRP3 or its downstream products as treatments for fibrotic disorders and discusses the connections between various NLRP3 activators and fibrosis.
Keywords: NLRP3 inflammasome; fibrosis; IL-1β; IL-18; calcium; potassium; therapeutics
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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