ArticleThe Journal of clinical investigation2016
Matricellular protein CCN3 mitigates abdominal aortic aneurysm.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- DNA Methylation-Guided Prediction and Validation of TAAD Molecular Targets.Biochemical genetics · 2026Article
- Fibrinogen-Bmal1 signaling as a therapeutic target to limit aortic dissection by preserving VSMC contractility.Signal transduction and targeted therapy · 2026Article
- Circulating Plasma Proteins Influence the Risk of Aortic Dissection via Blood Pressure: A Network Mendelian Randomization and Multi-Omics Study.Journal of inflammation research · 2026Article
- PRDM16 deficiency in vascular smooth muscle cells aggravates abdominal aortic aneurysm.JCI insight · 2023Article
- Myofibroblast Ccn3 is regulated by Yap and Wwtr1 and contributes to adverse cardiac outcomes.Frontiers in cardiovascular medicine · 2023Article
- Trimethylamine N-Oxide Promotes Abdominal Aortic Aneurysm Formation by Aggravating Aortic Smooth Muscle Cell Senescence in Mice.Journal of cardiovascular translational research · 2022Article
- Activating α7nAChR ameliorates abdominal aortic aneurysm through inhibiting pyroptosis mediated by NLRP3 inflammasome.Acta pharmacologica Sinica · 2022Article
- Molecular and Genetic Interactions between CCN2 and CCN3 behind Their Yin-Yang Collaboration.International journal of molecular sciences · 2022Review
- Artificial Intelligence Uncovers Natural MMP Inhibitor Crocin as a Potential Treatment of Thoracic Aortic Aneurysm and Dissection.Frontiers in cardiovascular medicine · 2022Article
- Vascular Smooth Muscle Cells in Aortic Aneurysm: From Genetics to Mechanisms.Journal of the American Heart Association · 2021Article
- Cellular communication network factor 3 in cartilage development and maintenance.Journal of cell communication and signaling · 2021Review
- Aneurysm severity is suppressed by deletion of CCN4.Journal of cell communication and signaling · 2021Article
- Cartilage oligomeric matrix protein is an endogenous β-arrestin-2-selective allosteric modulator of AT1 receptor counteracting vascular injury.Cell research · 2021Article
- Inhibition of Sphingosine-1-Phosphate Receptor 2 Prevents Thoracic Aortic Dissection and Rupture.Frontiers in cardiovascular medicine · 2021Article
- Chronic Intermittent Hypoxia Regulates CaMKII-Dependent MAPK Signaling to Promote the Initiation of Abdominal Aortic Aneurysm.Oxidative medicine and cellular longevity · 2021Article
- Article
- BAF60a Deficiency in Vascular Smooth Muscle Cells Prevents Abdominal Aortic Aneurysm by Reducing Inflammation and Extracellular Matrix Degradation.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Functional Vascular Tissue Engineering Inspired by Matricellular Proteins.Frontiers in cardiovascular medicine · 2019Review
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Myeloid deficiency of CCN3 exacerbates liver injury in a mouse model of nonalcoholic fatty liver disease.Journal of cell communication and signaling · 2018Article
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 5 countries.
Funding
Abstract
Abdominal aortic aneurysm (AAA) is a major cause of morbidity and mortality; however, the mechanisms that are involved in disease initiation and progression are incompletely understood. Extracellular matrix proteins play an integral role in modulating vascular homeostasis in health and disease. Here, we determined that the expression of the matricellular protein CCN3 is strongly reduced in rodent AAA models, including angiotensin II-induced AAA and elastase perfusion-stimulated AAA. CCN3 levels were also reduced in human AAA biopsies compared with those in controls. In murine models of induced AAA, germline deletion of Ccn3 resulted in severe phenotypes characterized by elastin fragmentation, vessel dilation, vascular inflammation, dissection, heightened ROS generation, and smooth muscle cell loss. Conversely, overexpression of CCN3 mitigated both elastase- and angiotensin II-induced AAA formation in mice. BM transplantation experiments suggested that the AAA phenotype of CCN3-deficient mice is intrinsic to the vasculature, as AAA was not exacerbated in WT animals that received CCN3-deficient BM and WT BM did not reduce AAA severity in CCN3-deficient mice. Genetic and pharmacological approaches implicated the ERK1/2 pathway as a critical regulator of CCN3-dependent AAA development. Together, these results demonstrate that CCN3 is a nodal regulator in AAA biology and identify CCN3 as a potential therapeutic target for vascular disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.