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
- Cardiac fibrosis is a defining pathological feature of diabetic cardiomyopathy (DCM), and excessive activation of cardiac fibroblasts plays a critical role in regulating cardiomyocyte function through paracrine signaling. CCN1 (cellular communication network factor 1), an extracellular matrix protein involved in intercellular communication, has been suggested to influence cardiac remodeling, although its specific impact on cardiomyocytes in DCM has remained unclear. In this study, we found that CCN1 expression was markedly elevated in cardiac tissues from DCM mouse models and in insulin-resistant cell models, with fibroblasts serving as the primary source. Proteomic analysis and co-culture experiments demonstrated that CCN1 suppressed cardiomyocyte macroautophagy/autophagy. To determine its role in vivo, we generated fibroblast-specific knockout mice and established a DCM model, demonstrating that deletion ameliorated cardiac dysfunction and restored autophagic activity. We further identified ITGAV-ITGB1/integrin αvβ1 as the receptor mediating CCN1 signaling in cardiomyocytes. Molecular dynamics simulations and co-immunoprecipitation experiments confirmed that CCN1 engaged ITGAV-ITGB1/integrin αvβ1 through its cysteine-knot-containing (CT) domain. Mechanistically, this interaction activated the downstream PTK2/FAK-MTOR signaling pathway, leading to inhibition of cardiomyocyte autophagy. Together, these findings reveal a previously unrecognized fibroblast-cardiomyocyte signaling axis in which fibroblast-derived CCN1 drives DCM progression by suppressing autophagy through ITGAV-ITGB1/integrin αvβ1-dependent signaling. This work provides mechanistic insight into the pathogenesis of DCM and identifies CCN1 as a potential therapeutic target for mitigating disease onset and progression. - Source: PubMed
Publication date: 2026/04/29
Hu Bo-AngZhang LeiSong MingKong Yan-RuJiao Ya-QiongJia XuZhu PingLi Yu-LinTi YunZhang WeiWang Zhi-HaoZhong Ming - Acute kidney injury (AKI) is driven by maladaptive tubular responses, yet upstream regulators remain incompletely understood. Here, we identify phosphatidylinositol 4-kinase alpha (Pi4ka) as a critical determinant of proximal tubule cell (PTC) homeostasis and injury progression. PI4KA expression was reduced in human diseased kidneys and negatively correlated with renal function. Single-cell RNA sequencing in mouse models revealed that Pi4ka deficiency preferentially perturbs specific PTC states, including Slc34a1Ccn1, and Slc34a1Apob populations, which diverge along distinct maladaptive trajectories. From these trajectories we derived a 40-gene injury signature enriched for lysosome-associated pathways, and functional assays showed that lysosomal dysfunction is an early event linking Pi4ka loss to ER stress, impaired autophagy, and proteostasis disruption. Transcriptional network analysis identified Creb3l2 as a central regulator of lysosomal activation. Notably, Creb3l2 perturbation suppressed stress and cell-death programs while promoting transcriptional programs associated with repair and phospholipid metabolism. Ligand-receptor inference further indicated that Pi4ka-deficient PTCs shape a pro-inflammatory immune microenvironment via immunomodulatory gene activation, an effect abolished by Creb3l2 deletion. Collectively, these findings define a Pi4ka-lysosome-Creb3l2 axis that coordinates tubular injury, maladaptive remodeling, and immune activation, highlighting potential therapeutic targets to limit AKI progression. - Source: PubMed
Publication date: 2026/04/27
Chen ZhiminXie JingzhiWu ChengkunYe KengChen YueSong YankunMa HuabinWu JianfengChen LiXu Yanfang - Polycystic ovary syndrome (PCOS) affects 11%-13% of reproductive-age women worldwide and is pathologically associated with granulosa cell dysfunction. This study employed transcriptome sequencing of granulosa cells from PCOS patients and non-PCOS controls, followed by Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Gene Set Enrichment Analysis. Key differentially expressed genes were validated by quantitative real-time PCR. Transcriptome analysis identified 157 upregulated and 71 downregulated mRNAs in PCOS granulosa cells, with enrichment in PI3K-Akt, MAPK, and TGF-beta signaling pathways. Six genes-NPTX2, FN1, CCN1, IDH1, ZCCHC17, and CREG1-were confirmed by qRT-PCR. Protein-protein interaction network analysis identified FN1 as a central hub gene. FN1 knockdown in KGN cells suppressed proliferation, induced apoptosis, and caused G1 phase arrest, accompanied by reduced Akt phosphorylation and altered expression of cyclin D1, p21, and p27. These findings suggest a potential association between FN1 and granulosa cell proliferative dysregulation in PCOS, warranting validation in primary cells and models. - Source: PubMed
Publication date: 2026/04/24
Zhou KanHan WenquanWang QijieZhang YuWang Jiao - - Source: PubMed
Publication date: 2026/04/22
Cui Xiao-LinSong Lin-JieLi QianJia Zi-HengDai XiyongWang MengLv Yang-PingChen Shuai-JunZhang He-DeCheng Pei-PeiYe Shu-YiHu Shi-HeLian Chen-YueLiang Li-MeiYu FanHe Xin-LiangXiong LiangXiang FeiWang XiaorongYe HongMa Wan-Li - Established biomarkers are used for risk stratification after STEMI, but their relationship with cardiac magnetic resonance (CMR)-derived infarct characteristics at 30 days remains incompletely understood. Because 30-day CMR reflects an intermediate post-infarction stage between acute myocardial injury and the later chronic infarct state, we evaluated whether baseline high-sensitivity troponin T (hsTnT), N-terminal pro-B-type natriuretic peptide (NT-proBNP), cellular communication network factor 1 (CCN1), and proprotein convertase subtilisin/kexin type 9 (PCSK9) are associated with 30-day CMR parameters. - Source: PubMed
Publication date: 2026/04/12
Horbach TimWenzl Florian AManka RobertRäber LorenzCarballo DavidKeller TillSossalla SamuelRuschitzka Frankvon Eckardstein ArnoldStähli Barbara ELüscher Thomas FKlingenberg Roland