ArticleAmerican journal of hypertension2011
Proinflammatory protein CARD9 is essential for infiltration of monocytic fibroblast precursors and cardiac fibrosis caused by Angiotensin II infusion.
Article in American journal of hypertension, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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39 citing papers in PubMed, 62 citations in OpenAlex.
- Genetic Regulation of DNA Methylation and Its Mediating Role in Blood Pressure: A Genome-Wide Twin Study.MedComm · 2026Article
- Macrophage OTUD1-CARD9 axis drives isoproterenol-induced inflammatory heart remodelling.Clinical and translational medicine · 2024Article
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Macrophage CARD9 mediates cardiac injury following myocardial infarction through regulation of lipocalin 2 expression.Signal transduction and targeted therapy · 2023Article
- Genetic inhibition of CARD9 accelerates the development of atherosclerosis in mice through CD36 dependent-defective autophagy.Nature communications · 2023Article
- CARD9 deficiency improves the recovery of limb ischemia in mice with ambient fine particulate matter exposure.Frontiers in cardiovascular medicine · 2023Article
- Article
- CARD9 Signaling, Inflammation, and Diseases.Frontiers in immunology · 2022Review
- CARD9 Regulation and its Role in Cardiovascular Diseases.International journal of biological sciences · 2022Review
- Electroimmunology and cardiac arrhythmia.Nature reviews. Cardiology · 2021Review
- Complex Relationship Between Cardiac Fibroblasts and Cardiomyocytes in Health and Disease.Journal of the American Heart Association · 2021Review
- Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling.Frontiers in cell and developmental biology · 2021Review
- CARD9: key player or bystander in cardiac remodeling under hypertension?Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- Macrophage-derived extracellular vesicles: diverse mediators of pathology and therapeutics in multiple diseases.Cell death & disease · 2020Review
- The Role of CARD9 in Metabolic Diseases.Current medical science · 2020Review
- The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism.Chinese medicine · 2020Article
- KJournal of the American Heart Association · 2019Article
- Molecular and physiological roles of the adaptor protein CARD9 in immunity.Cell death & disease · 2018Review
- 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
- Macrophage-derived exosomes induce inflammatory factors in endothelial cells under hypertensive conditions.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Article
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10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAngiotensin II (Ang II)-induced cardiac remodeling with the underlying mechanisms involving inflammation and fibrosis has been well documented. Cytosolic adaptor caspase recruitment domain 9 (CARD9) has been implicated in the innate immune response. We aimed to examine the role of CARD9 in inflammation and cardiac fibrosis induced by Ang II.
methodsTwo-month-old CARD9-deficient (CARD9(-/-)) and wild-type (WT) male mice were infused with Ang II (1,500 ng/kg/min) or saline for 7 days. Heart sections were stained with hematoxylin and eosin and Masson trichrome and examined by immunohistochemistry; and activity and protein levels were measured in macrophages obtained from mice.
resultsWT mice with Ang II infusion showed a marked increase in CARD9(+) macrophages in the heart, but CARD9(-/-) mice showed significantly suppressed macrophage infiltration and expression of proinflammatory cytokines, including interleukin-1β (IL-1β) and connective tissue growth factor (CTGF). Importantly, Ang II-induced cardiac fibrosis (extracellular matrix and collagen I deposition) was diminished in CARD9(-/-) hearts, as was the expression of transforming growth factor-β (TGF-β) and level of myofibroblasts positive for α-smooth muscle actin (α-SMA). Furthermore, Ang II activation of nuclear factor-κB (NF-κB), JNK and p38 mitogen-activated protein kinases (MAPKs) in WT macrophages was reduced in CARD9(-/-) macrophages.
conclusionCARD9 plays an important role in regulating cardiac inflammation and fibrosis in response to elevated Ang II.
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