ArticleCirculation research2006
The matricellular protein CCN1 is essential for cardiac development.
Article in Circulation research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 110 citations in OpenAlex.
- O-GlcNAcylation as a Metabolic Integrator in Cardiovascular Physiology and Disease.International journal of molecular sciences · 2026Review
- Silicate biomaterials-based multicellular scaffolds with specific cellular spatial distribution for infarcted myocardium repair.Bioactive materials · 2026Article
- Cysteine-Rich Protein 61 (CCN1) Deficiency Alleviated Cardiac Remodeling in 5/6 Nephrectomized Mice by Suppressing the MAPK Signaling Pathway.Cardiovascular therapeutics · 2025Article
- Cardiac arrhythmia in individuals with steroid sulfatase deficiency (X-linked ichthyosis): candidate anatomical and biochemical pathways.Essays in biochemistry · 2024Review
- Paternal hypercholesterolemia elicits sex-specific exacerbation of atherosclerosis in offspring.JCI insight · 2024Article
- Hippo Signaling Mediates TGFβ-Dependent Transcriptional Inputs in Cardiac Cushion Mesenchymal Cells to Regulate Extracellular Matrix Remodeling.Journal of cardiovascular development and disease · 2023Article
- Why do humans need thrombospondin-1?Journal of cell communication and signaling · 2023Review
- Structural insights into regulation of CCN protein activities and functions.Journal of cell communication and signaling · 2023Review
- The regulation and functions of the matricellular CCN proteins induced by shear stress.Journal of cell communication and signaling · 2023Review
- CCN1 interacts with integrins to regulate intestinal stem cell proliferation and differentiation.Nature communications · 2022Article
- CCN1 Promotes Inflammation by Inducing IL-6 ProductionFrontiers in immunology · 2022Article
- CCN1 gene polymorphisms associated with congenital heart disease susceptibility in Northwest Chinese population from different high-altitude areas.Environmental science and pollution research international · 2021Article
- Association between CCN1 gene polymorphism and acute coronary syndrome in Chinese Han and Uygur populations.Hereditas · 2021Article
- Differential intolerance to loss of function and missense mutations in genes that encode human matricellular proteins.Journal of cell communication and signaling · 2021Article
- Dickkopf‑1/cysteine‑rich angiogenic inducer 61 axis mediates palmitic acid‑induced inflammation and apoptosis of vascular endothelial cells.Molecular medicine reports · 2021Article
- The Roles of CCN1/CYR61 in Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Eyeing the Extracellular Matrix in Vascular Development and Microvascular Diseases and Bridging the Divide between Vascular Mechanics and Function.International journal of molecular sciences · 2020Review
- Caught between a "Rho" and a hard place: are CCN1/CYR61 and CCN2/CTGF the arbiters of microvascular stiffness?Journal of cell communication and signaling · 2020Review
- Genetics of Congenital Heart Disease.Biomolecules · 2019Review
- ADAMTS9 and ADAMTS20 are differentially affected by loss of B3GLCT in mouse model of Peters plus syndrome.Human molecular genetics · 2019Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The matricellular protein CCN1 (formerly named CYR61) regulates cell adhesion, migration, proliferation, survival, and differentiation through binding to integrin receptors and heparan sulfate proteoglycans. Here we show that Ccn1-null mice are impaired in cardiac valvuloseptal morphogenesis, resulting in severe atrioventricular septal defects (AVSD). Remarkably, haploinsufficiency for Ccn1 also results in delayed formation of the ventricular septum in the embryo and persistent ostium primum atrial septal defects (ASD) in approximately 20% of adults. Mechanistically, Ccn1 is not required for epithelial-to-mesenchymal transformation or cell proliferation and differentiation in the endocardial cushion tissue. However, Ccn1 deficiency leads to precocious apoptosis in the atrial junction of the cushion tissue and impaired gelatinase activities in the muscular component of the interventricular septum at embryonic day 12.5, when fusion between the endocardial cushion tissue and the atrial and ventricular septa occurs, indicating that these defects may underlie the observed AVSD. Moreover, human CCN1 maps to 1p21-p31, the chromosomal location of an AVSD susceptibility gene. Together, these results provide evidence that deficiency in matrix signaling can lead to autosomal dominant AVSD, identify Ccn1(+/-) mice as a genetic model for ostium primum ASD, and implicate CCN1 as a candidate gene for AVSD in humans.
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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.