NLRP3 Inflammasome in Atherosclerosis: Putting Out the Fire of Inflammation
Atherosclerosis (AS) is a chronic inflammatory disease with thickening or hardening of the arteries, which led to the built-up of plaques in the inner lining of an artery. Among all the clarified pathogenesis, the over-activation of inflammatory reaction is one of the most acknowledged one. The nucl...
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| Veröffentlicht in: | Inflammation 2023-02, Vol.46 (1), p.35-46 |
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| creator | Shao, Bo-Zong Xu, Hai-Yan Zhao, Yi-Cheng Zheng, Xiao-Rui Wang, Fang Zhao, Guan-Ren |
| description | Atherosclerosis (AS) is a chronic inflammatory disease with thickening or hardening of the arteries, which led to the built-up of plaques in the inner lining of an artery. Among all the clarified pathogenesis, the over-activation of inflammatory reaction is one of the most acknowledged one. The nucleotide-binding domain leucine-rich repeat (NLR) and pyrin domain containing receptor 3 (NLRP3) inflammasome, as a vital and special form of inflammation and innate immunity, has been widely revealed to participate in the onset and development of AS. This review will introduce the process of the pathogenesis and progression of AS, and will describe the biological features of the NLRP3 inflammasome. Furthermore, the role of the NLRP3 inflammasome in AS and the possible mechanisms will be discussed. In addition, several kinds of agents with the effect of anti-atherosclerotic taking advantage of the NLRP3 inflammasome intervention will be described and discussed in detail, including natural compounds (baicalin, dihydromyricetin, luteolin, 5-deoxy-rutaecarpine (R3) and Salvianolic acid A, etc.), microRNAs (microRNA-30c-5p, microRNA-9, microRNA-146a-5p, microRNA-16-5p and microRNA-181a, etc.), and autophagy regulators (melatonin, dietary PUFA and arglabin, etc.). We aim to provide novel insights in the exploration of the specific mechanisms of AS and the development of new treatments of AS. |
| doi_str_mv | 10.1007/s10753-022-01725-x |
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Among all the clarified pathogenesis, the over-activation of inflammatory reaction is one of the most acknowledged one. The nucleotide-binding domain leucine-rich repeat (NLR) and pyrin domain containing receptor 3 (NLRP3) inflammasome, as a vital and special form of inflammation and innate immunity, has been widely revealed to participate in the onset and development of AS. This review will introduce the process of the pathogenesis and progression of AS, and will describe the biological features of the NLRP3 inflammasome. Furthermore, the role of the NLRP3 inflammasome in AS and the possible mechanisms will be discussed. In addition, several kinds of agents with the effect of anti-atherosclerotic taking advantage of the NLRP3 inflammasome intervention will be described and discussed in detail, including natural compounds (baicalin, dihydromyricetin, luteolin, 5-deoxy-rutaecarpine (R3) and Salvianolic acid A, etc.), microRNAs (microRNA-30c-5p, microRNA-9, microRNA-146a-5p, microRNA-16-5p and microRNA-181a, etc.), and autophagy regulators (melatonin, dietary PUFA and arglabin, etc.). We aim to provide novel insights in the exploration of the specific mechanisms of AS and the development of new treatments of AS.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-022-01725-x</identifier><identifier>PMID: 35953687</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Arteries ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - pathology ; Autophagy ; Baicalin ; Biomedical and Life Sciences ; Biomedicine ; Humans ; Immunology ; Inflammasomes ; Inflammation - pathology ; Inflammatory diseases ; Innate immunity ; Internal Medicine ; MicroRNAs ; miRNA ; NLR Family, Pyrin Domain-Containing 3 Protein ; Pathogenesis ; Pathology ; Pharmacology/Toxicology ; Pyrin protein ; Review ; Rheumatology</subject><ispartof>Inflammation, 2023-02, Vol.46 (1), p.35-46</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. 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In addition, several kinds of agents with the effect of anti-atherosclerotic taking advantage of the NLRP3 inflammasome intervention will be described and discussed in detail, including natural compounds (baicalin, dihydromyricetin, luteolin, 5-deoxy-rutaecarpine (R3) and Salvianolic acid A, etc.), microRNAs (microRNA-30c-5p, microRNA-9, microRNA-146a-5p, microRNA-16-5p and microRNA-181a, etc.), and autophagy regulators (melatonin, dietary PUFA and arglabin, etc.). We aim to provide novel insights in the exploration of the specific mechanisms of AS and the development of new treatments of AS.</description><subject>Arteries</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - pathology</subject><subject>Autophagy</subject><subject>Baicalin</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Humans</subject><subject>Immunology</subject><subject>Inflammasomes</subject><subject>Inflammation - pathology</subject><subject>Inflammatory diseases</subject><subject>Innate immunity</subject><subject>Internal Medicine</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Pyrin protein</subject><subject>Review</subject><subject>Rheumatology</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kD1PwzAURS0EoqXwBxhQJBaWgD_iPJutqihUVLRCMFtOYpdU-ShxIpV_j0sKSAws9vDOvX4-CJ0TfE0whhtHMHAWYkpDTIDycHuAhoQDCymH-BANMYtxyKSEATpxbo0xFlKwYzRgXHIWCxiix6f585IFs8oWuiy1q0sT5FUwbt9MU7u02J25uw2WXdvm1SpYdG3gZ8E0b0xQ259gm9fVKTqyunDmbH-P0Ov07mXyEM4X97PJeB6mDHgbgjZRbFPNIyuzWEJEUyNllOjEamwAkoRoKmLGY2ltFHGSCZPENDOQ2UiDYCN01fdumvq9M65VZe5SUxS6MnXnFAVMiaRMcI9e_kHXdddUfjtPCUwjQQA8RXsq9b91jbFq0-Slbj4UwWqnWvWqlVetvlSrrQ9d7Ku7pDTZT-TbrQdYDzg_qlam-X37n9pPMQmJRQ</recordid><startdate>20230201</startdate><enddate>20230201</enddate><creator>Shao, Bo-Zong</creator><creator>Xu, Hai-Yan</creator><creator>Zhao, Yi-Cheng</creator><creator>Zheng, Xiao-Rui</creator><creator>Wang, Fang</creator><creator>Zhao, Guan-Ren</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20230201</creationdate><title>NLRP3 Inflammasome in Atherosclerosis: Putting Out the Fire of Inflammation</title><author>Shao, Bo-Zong ; 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| subjects | Arteries Arteriosclerosis Atherosclerosis Atherosclerosis - pathology Autophagy Baicalin Biomedical and Life Sciences Biomedicine Humans Immunology Inflammasomes Inflammation - pathology Inflammatory diseases Innate immunity Internal Medicine MicroRNAs miRNA NLR Family, Pyrin Domain-Containing 3 Protein Pathogenesis Pathology Pharmacology/Toxicology Pyrin protein Review Rheumatology |
| title | NLRP3 Inflammasome in Atherosclerosis: Putting Out the Fire of Inflammation |
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