ArticleCardiovascular research2015
CARD9 mediates necrotic smooth muscle cell-induced inflammation in macrophages contributing to neointima formation of vein grafts.
Article in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Vps16 Attenuates Myocardial Ischemia/reperfusion Injury by Interacting with UVRAG and Activating Rab7.Cardiovascular drugs and therapy · 2026Article
- Ubiquitin Specific Protease 9X Regulates the Activation of ARK5 and Promotes Progression of Fibrotic Remodeling.JACC. Basic to translational science · 2025Article
- Nanomedicine-based strategies for the treatment of vein graft disease.Nature reviews. Cardiology · 2025Review
- Macrophage CARD9 mediates cardiac injury following myocardial infarction through regulation of lipocalin 2 expression.Signal transduction and targeted therapy · 2023Article
- CARD9 Signaling, Inflammation, and Diseases.Frontiers in immunology · 2022Review
- CARD9 Regulation and its Role in Cardiovascular Diseases.International journal of biological sciences · 2022Review
- The Role of CARD9 in Metabolic Diseases.Current medical science · 2020Review
- Deletion of hematopoietic Dectin-2 or CARD9 does not protect against atherosclerotic plaque formation in hyperlipidemic mice.Scientific reports · 2019Article
- Epigenetics and Immunometabolism in Diabetes and Aging.Antioxidants & redox signaling · 2018Review
- Hyperacute Monocyte Gene Response Patterns Are Associated With Lower Extremity Vein Bypass Graft Failure.Circulation. Genomic and precision medicine · 2018Article
- Molecular and physiological roles of the adaptor protein CARD9 in immunity.Cell death & disease · 2018Review
- Tumor necrosis factor alpha-stimulated gene-6 (TSG-6) inhibits the inflammatory response by inhibiting the activation of P38 and JNK signaling pathway and decreases the restenosis of vein grafts in rats.Heart and vessels · 2017Article
- Zinc rescues obesity-induced cardiac hypertrophy via stimulating metallothionein to suppress oxidative stress-activated BCL10/CARD9/p38 MAPK pathway.Journal of cellular and molecular medicine · 2017Article
- Label-free LC-MS/MS shotgun proteomics to investigate the anti-inflammatory effect of rCC16.Molecular medicine reports · 2016Article
- CARD9 as a potential target in cardiovascular disease.Drug design, development and therapy · 2016Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
aimsInflammation plays an important role in the neointima formation of grafted veins. However, the initiation of inflammation in grafted veins is still unclear. Here, we investigated the role and underlying mechanism of an innate immunity signalling protein, caspase-associated recruitment domain 9 (CARD9) in vein grafts in mice. METHODS AND
resultsIn early murine vein grafts, we observed robust death of smooth muscle cells (SMCs), which was accompanied by infiltration of macrophages and expression of pro-inflammatory cytokines. Meanwhile, SMC necrosis was associated with the expression of pro-inflammatory cytokines in macrophages in vitro. To explore the mediators of necrotic SMC-induced inflammation in grafted veins from mice, we examined the expression of CARD family proteins and found CARD9 highly expressed in infiltrated macrophages of grafted veins. CARD9-knockout (KO) inhibited necrotic SMC-induced pro-inflammatory cytokine expression and NF-κB activation. Furthermore, CARD9-KO suppressed necrotic SMC-induced expression of VEGF in macrophages. Finally, CARD9-KO decreased neointima formation of grafted veins in mice.
conclusionThe innate immune protein CARD9 in macrophages may mediate necrotic SMC-induced inflammation by activating NF-κB and contributed to neointima formation in the vein grafts.
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