The Role of CARD9 in Metabolic Diseases

Tian, Cheng; Tuo, Yali; Lu, Yi; Xu, Cenke; Xiang, Ming

doi:10.1007/s11596-020-2166-4

Cited by 12 publications

(14 citation statements)

References 59 publications

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“…It has been well established that excessive inflammation, ROS production and related oxidative stress significantly contribute to CVDs, including atherosclerosis, cardiac fibrosis, coronary artery disease, myocardial infarction, and heart failure ( 4 , 6 , 86 , 149 ). CARD9-mediated signaling in CVDs has been well documented in several reviews ( 4 , 16 , 150 ). Briefly, CARD9-mediated production of cytokines and chemokines results in cardiovascular dysfunction by instigating a positive feedback loop of inflammation and oxidative stress.…”

Section: Card9 and Diseasesmentioning

confidence: 98%

“…Reactive oxygen species (ROS) formation and oxidative stress are closely related to the development and progression of a variety of diseases including infection, inflammatory diseases, tumors, and cardiovascular diseases (CVDs) ( 12 – 14 ). The critical roles of CARD9 in cytokines/chemokines secretion and ROS production in different cells and organ systems naturally connect CARD9 with the disease conditions associated with ROS and inflammation ( 4 , 9 , 15 , 16 ). Mutation and genetic polymorphisms of CARD9 are reported to be correlated with a wide range of infectious diseases in human ( 17 – 19 ).…”

Section: Introductionmentioning

confidence: 99%

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CARD9 Signaling, Inflammation, and Diseases

et al. 2022

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Caspase-recruitment domain 9 (CARD9) protein is expressed in many cells especially in immune cells, and is critically involved in the function of the innate and adaptive immune systems through extensive interactions between CARD9 and other signaling molecules including NF-κB and MAPK. CARD9-mediated signaling plays a central role in regulating inflammatory responses and oxidative stress through the productions of important cytokines and chemokines. Abnormalities of CARD9 and CARD9 signaling or CARD9 mutations or polymorphism are associated with a variety of pathological conditions including infections, inflammation, and autoimmune disorders. This review focuses on the function of CARD9 and CARD9-mediated signaling pathways, as well as interactions with other important signaling molecules in different cell types and the relations to specific disease conditions including inflammatory diseases, infections, tumorigenesis, and cardiovascular pathologies.

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Section: Card9 and Diseasesmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

CARD9 Signaling, Inflammation, and Diseases

et al. 2022

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“…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 - 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 . In contrast, we focus on the various potential roles of CARD9 in CVDs from different perspectives based on recent studies.…”

Section: Introductionmentioning

confidence: 99%

CARD9 Regulation and its Role in Cardiovascular Diseases

Zhang¹,

Wang²,

Men³

et al. 2022

Int. J. Biol. Sci.

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Caspase recruitment domain-containing protein 9 (CARD9) is an adaptor protein expressed on myeloid cells and located downstream of pattern recognition receptors (PRRs), which transduces signals involved in innate immunity. CARD9 deficiency is associated with increased susceptibility to various fungal diseases. Increasing evidence shows that CARD9 mediates the activation of p38 MAPK, NF-κB, and NLRP3 inflammasome in various CVDs and then promotes the production of proinflammatory cytokines and chemokines, which contribute to cardiac remodeling and cardiac dysfunction in certain cardiovascular diseases (CVDs). Moreover, CARD9-mediated anti-apoptosis and autophagy are implicated in the progression of CVDs. Here, we summarize the structure and function of CARD9 in innate immunity and its various roles in inflammation, apoptosis, and autophagy in the pathogenesis of CVDs. Furthermore, we discuss the potential therapies targeting CARD9 to prevent CVDs and raise some issues for further exploring the role of CARD9 in CVDs.

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“…Animal studies have shown that global CARD9-deficient mice are resistant to developing viral myocarditis, cardiac hypertrophy, or vein graft failure. 3 CARD9 expression is significantly increased in viral myocarditis, and CARD9 deficiency prevents Coxsackie virus B3-induced excessive inflammation and production of transforming growth factor-β (TGF-β), IL-17A, and BCL-10 in mouse myocardium, with decreased serum levels of IL-6, IL-10, IFN-γ, TGF-β, and IL-17A. Angiotensin II and transverse aortic constriction markedly increase CARD9 expression in the mouse heart.…”

mentioning

confidence: 99%

“…High-fat diet and zinc deficiency-induced oxidative stress activate CARD9/p38 MAPK signaling, an important mechanism for obesity-related cardiac hypertrophy. 3 Zinc supplement suppresses CARD9 expression and reduces oxidative stress in mice on a high-fat diet. CARD9 expression and production of proinflammatory cytokines are increased in vein grafts and associated with graft macrophage infiltration and neointima formation.…”

mentioning

confidence: 99%