Ask about this productRelated genes to: CYR61 protein
- Gene:
- CCN1 NIH gene
- Name:
- cellular communication network factor 1
- Previous symbol:
- IGFBP10, CYR61
- Synonyms:
- GIG1
- Chromosome:
- 1p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-02
- Date modifiied:
- 2018-10-11
Related products to: CYR61 protein
Related articles to: CYR61 protein
- Maternal vascular dysfunction and impaired placental angiogenesis are key features of preeclampsia (PE). Umbilical cord blood-derived endothelial colony-forming cells (CB-ECFCs) contribute to fetal endothelial repair and vascular network formation, but their phenotype in PE remains incompletely understood. - Source: PubMed
Publication date: 2026/08/28
Ma YuyangYang FenglianWang YuLi YingyaJia YanpingWang JieLi KunmingDuan Liyan - Circulating cellular communication network factor 1 (CCN1) improves risk stratification in patients with acute coronary syndrome. We here investigated the association of CCN1 with all-cause mortality in patients with dilated cardiomyopathy (DCM). - Source: PubMed
Publication date: 2026/08/29
Klingenberg RolandGross StefanLehnert KristinGrote KarstenBenkner AlexanderWegner DaniloHamm Christian WFelix Stephan BKeller TillPankuweit SabineDörr Marcus - Connective tissue growth factor (CTGF), also known as CCN2, is a matricellular protein of the CCN family (CCN1-6) that regulates the proliferation of vascular smooth muscle cells (VSMCs), thereby contributing to the pathogenesis of atherosclerosis and hypertension. However, the intercellular signaling pathway that CTGF takes for vascular remodeling, such as VSMC phenotype transition, has not been fully elucidated. This study employed a combination of in vivo and in vitro tests to examine VSMC phenotype and reveal the role of CTGF in vascular remodeling induced by angiotensin II (Ang II). The in vitro experiments showed that Ang II upregulated CTGF expression in rat VSMCs in a concentration- and time-dependent manner. Genetic depletion of CTGF with siRNA against rat Ccn2 prevented Ang II-induced autophagic flux impairment. In addition, Ang II-induced phenotypic switch was inhibited by 3-MA, an inhibitor of autophagy, suggesting CTGF is involved in Ang II-induced phenotypic switch via regulating autophagic flux impairment. In addition, this CTGF-dependent autophagy regulation was involved in Ang II-induced mitochondrial dysfunction in VSMCs. Moreover, anti-CTGF antibody treatment inhibited neointimal hyperplasia in a mouse model of carotid artery ligation-induced neointima formation suggesting a novel perspective role of CTGF in the phenotype switching of VSMCs and the neointimal proliferation process. These results offer insights into the effect of anti-CTGF on preventing autophagic flux impairment and VSMC phenotype switching caused by mitochondrial dysfunction in vascular diseases associated with aberrant VSMC proliferation. - Source: PubMed
Hwang Ae-RangWoo Chang-HoonKang Young Jin - Cellular communication network factor 1 (CCN1) is a secreted matricellular protein induced by growth factors, mechanical stress, hypoxia, and tissue injury and regulates diverse cellular processes through interactions with integrins, heparan sulfate proteoglycans, and extracellular matrix (ECM) components. Although prior reviews have broadly summarized CCN1 biology, its potential as a biomarker warrants a more focused synthesis of empirical evidence. Here, we propose that CCN1 should be viewed not as a generic disease marker, but as a compartment-specific biomarker of active microenvironmental remodeling. Emerging evidence identifies CCN1 as a central regulator of bone pathology and cancer progression, functioning at the intersection of osteogenesis, osteolysis, angiogenesis, stromal remodeling, immune modulation, and metastatic colonization. Within the skeletal niche, CCN1 is produced by tumor cells, stromal fibroblasts, endothelial cells, and bone-resident cells, where it influences osteoblast and osteoclast activity and promotes vascular niche formation. CCN1 also participates in fracture repair, bone marrow mesenchymal stem cell aging, epithelial-mesenchymal transition, and tumor dissemination, highlighting its roles in both regenerative and pathological processes. Importantly, CCN1 exists in distinct biological compartments, including ECM-bound, soluble circulating, extracellular vesicle-associated, and tumor cell-associated pools. These compartments likely convey different biological information, ranging from local osteogenic to systemic injury, inflammation, and metastatic spread. While circulating CCN1 is measurable and shows promise as a minimally invasive biomarker, its interpretation must account for disease context, timing, and biological compartment. We conclude that CCN1 represents a compelling translational candidate linking bone remodeling and cancer biology, with future studies needed to validate its biomarker utility in skeletal disease and metastasis. - Source: PubMed
Publication date: 2026/08/18
Tran Angela BOrtiz-Hernandez Greisha L - The present study evaluated the effect of short-term feeding with graded dietary protein levels on skin wound healing in largemouth bass (Micropterus salmoides). Three isolipidic diets containing 48% (P48), 52% (P52), and 56% (P56) crude protein were fed to fish (initial mean weight 13.00 g) for 5 weeks, followed by a standardized mechanical skin-wounding challenge. Wound repair was assessed at 1, 3, and 7 days post-wounding (dpw). The P52 diet supported better growth performance than the P48 diet. However, P48 accelerated wound closure and promoted more advanced histological repair, characterized by earlier re-epithelialization, more efficient necrotic tissue clearance, reduced wound bed area, and a thinner, more mature neo-epidermis. At the molecular level, P48 induced early upregulation of re-epithelialization-related genes, including mmp2, mmp9, and egf, accompanied by stronger MMP9 immunohistochemical signals. P48 was also associated with rapid inflammatory activation, shown by early increases in MPO, NAG, and LZM activities and il1b and tnfa expression, followed by faster inflammatory resolution and sustained il10 upregulation. In addition, P48 showed higher antimicrobial-defense-related markers and stronger extracellular-matrix-, angiogenesis-, and collagen-associated responses, as evidenced by higher expression of hamp, prf, fn1, lamb2, vegf, shh, and col1a1, stronger CD31-positive immunofluorescence signals, and greater collagen fiber accumulation. Western blotting further showed that FN1, SHH, and CCN1 protein responses were broadly consistent with their corresponding transcript-level patterns. Temporal response analysis further indicated a coordinated transition from early epithelial and inflammatory responses to later repair and remodeling responses. Correlation analysis showed that reduced wound area was significantly and negatively associated with both ccn1 transcript abundance and CCN1 protein abundance. These findings indicate that short-term low-protein feeding enhances skin wound healing and may represent a stage-specific nutritional strategy for farmed largemouth bass. - Source: PubMed
Publication date: 2026/09/01
Chen ZhichuDing ZijianWang YiLiu ChanglinLiu JingyangLin JingruYe DingliEsteban María ÁngelesZhang YanjiaoZhang Dianguang