Journal
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2023.1149911
Keywords
viral myocarditis; inflammasome; infection; cytokines; interleukin-1 beta
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Viral myocarditis (VMC) is a life-threatening disease caused by viral infection-induced inflammation, which is associated with dilated cardiomyopathy or heart failure. Innate immunity plays a crucial role in the inflammation, with inflammasomes providing a platform for cytokine secretion and mediating pyroptosis. In this review, we summarized the pathways involving inflammasomes in VMC and discussed potential therapies targeting inflammasomes and related pathways.
Viral myocarditis (VMC), characterized by viral infection-induced inflammation, is a life-threatening disease associated with dilated cardiomyopathy or heart failure. Innate immunity plays a crucial role in the progression of inflammation, in which inflammasomes provide a platform for the secretion of cytokines and mediate pyroptosis. Inflammasomes are rising stars gaining increasing attention. The nucleotide oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3 (NLRP3) inflammasome, the caspase recruitment domain-containing protein 8 (CARD8) inflammasome, and the caspase-11 inflammasome are three inflammasomes that were reported to affect the process and prognosis of VMC. These inflammasomes can be activated by a wide range of cellular events. Accumulating evidence has suggested that inflammasomes are involved in different stages of VMC, including the trigger and progression of myocardial injury and remodeling after infection. In this review, we summarized the pathways involving inflammasomes in VMC and discussed the potential therapies targeting inflammasomes and related pathways.
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