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2020
DOI: 10.1016/j.carpath.2020.107261
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CARD9 mediates T cell inflammatory response in Coxsackievirus B3-induced acute myocarditis

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Cited by 8 publications
(9 citation statements)
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“…Therefore, inhibition of CARD9 signaling has been considered as a potential therapeutic strategy to the prevention and treatment of CVDs ( 4 ). Indeed, CARD9 deletion has been shown to prevent Coxsackievirus B3 (CVB3)-induced acute myocarditis ( 151 ), Candida albicans water-soluble extract (CAWS)-induced vasculitis ( 152 ), neointima formation of grafted veins ( 153 ), as well as TAC- or Angiotensin II (Ang II)-induced cardiac dysfunction, fibrosis, and hypertrophy ( 85 , 154 ), through attenuation of NF-κB, JNK and p38 MAPKs pathway, and production of various cytokines, such as IL-6, IL-1β, TNF-α, IL-17A, TGF-β, and IFN-γ. However, deletion of hematopoietic CARD9 shows no protective effects on atherosclerosis, probably because of no significant reduction of cytokines secretion (IL-6 and TNF-α) or mRNA expressions (IL-1β, IL-10, TNF-α, and MCP-1) ( 149 , 155 ).…”
Section: Card9 and Diseasesmentioning
confidence: 99%
“…Therefore, inhibition of CARD9 signaling has been considered as a potential therapeutic strategy to the prevention and treatment of CVDs ( 4 ). Indeed, CARD9 deletion has been shown to prevent Coxsackievirus B3 (CVB3)-induced acute myocarditis ( 151 ), Candida albicans water-soluble extract (CAWS)-induced vasculitis ( 152 ), neointima formation of grafted veins ( 153 ), as well as TAC- or Angiotensin II (Ang II)-induced cardiac dysfunction, fibrosis, and hypertrophy ( 85 , 154 ), through attenuation of NF-κB, JNK and p38 MAPKs pathway, and production of various cytokines, such as IL-6, IL-1β, TNF-α, IL-17A, TGF-β, and IFN-γ. However, deletion of hematopoietic CARD9 shows no protective effects on atherosclerosis, probably because of no significant reduction of cytokines secretion (IL-6 and TNF-α) or mRNA expressions (IL-1β, IL-10, TNF-α, and MCP-1) ( 149 , 155 ).…”
Section: Card9 and Diseasesmentioning
confidence: 99%
“…Moreover, they still confirmed that CARD9 deficiency did not affect the initiation of CD8 + T cell response. In a Coxsackievirus B3 (CVB3)-induced viral myocarditis mouse model, CARD9 deletion downregulated the mRNA and protein expression of TGF-β, IL-17A, and BCL-10, thereby ameliorating the CARD9-involved potent inflammation response (Sun et al, 2020 ). Based on these, a conflicting effect of CARD9 in viral infection is unfolding before our eyes.…”
Section: Virusesmentioning
confidence: 99%
“…As detected in infectious models of acute viral myocarditis and cardiac arteritis 38 , 39 , PAMPs can induce immune responses that cause acute myocardial injury. In myocarditis induced by coxsackievirus B3 (CVB3), a single-stranded RNA virus, CARD9 -knockout (KO) mice showed less myocardial inflammation and structural disorganization 10 . In addition, CARD9 -KO mice were also protected from Candida albicans water-soluble extract (CAWS)-induced cardiac vasculitis, as evidenced by decreased vascular inflammation score 39 .…”
Section: Evidence For the Role Of Card9 In Cvdsmentioning
confidence: 99%
“…Clinically, CARD9 singlenucleotide polymorphisms have been found to be involved in autoimmune diseases, such as Crohn's disease, ulcerative colitis, ankylosing spondylitis, IgA nephropathy, and rheumatoid arthritis [6][7][8][9]. In fact, CARD9 also plays a role in both infectious and non-infectious pathophysiological processes of heart injuries, including myocarditis, myocardial ischemia reperfusion (I/R) injury, and angiotensin II (Ang II)-induced cardiac remodeling and dysfunction [10][11][12]. Previously, Tian et al summarized the proinflammatory role of CARD9 in metabolic diseases, including insulin resistance and obesity, which are the risk factors of CVDs, and in heart diseases [13].…”
Section: Introductionmentioning
confidence: 99%