ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
CYR61 (CCN1) overexpression induces lung injury in mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis.Advances in respiratory medicine · 2023Pooled it
- Alveolar-Basal Intermediates Drive Pulmonary Fibrosis via Coordination of a Pro-Fibrotic Signaling Niche in Silicosis.bioRxiv : the preprint server for biology · 2026Article
- Article
- Cysteine-rich 61 inhibition attenuates hepatic insulin resistance and improves lipid metabolism in high-fat diet fed mice and HepG2 cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- NLRP3 inflammasome mediates abnormal epithelial regeneration and distal lung remodeling in silica‑induced lung fibrosis.International journal of molecular medicine · 2024Article
- Back to the future: targeting the extracellular matrix to treat systemic sclerosis.Nature reviews. Rheumatology · 2023Review
- Molecular insights using spatial transcriptomics of the distal lung in congenital diaphragmatic hernia.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Astragaloside IV improves pulmonary arterial hypertension by increasing the expression of CCN1 and activating the ERK1/2 pathway.Journal of cellular and molecular medicine · 2023Article
- Highway toFrontiers in pharmacology · 2022Review
- Construction and Validation of a Novel Prognostic Signature of Idiopathic Pulmonary Fibrosis by Identifying Subtypes Based on Genes Related to 7-Methylguanosine Modification.Frontiers in genetics · 2022Article
- Cyr61 Alleviates Cholangitis by Inhibiting Cytotoxic Effects of CD8Current medical science · 2021Article
- Serum CYR61 Is Associated With Airway Inflammation and Is a Potential Biomarker for Severity in Chronic Obstructive Pulmonary Disease.Frontiers in medicine · 2021Article
- The Role of Innate Immunity in Pulmonary Infections.BioMed research international · 2021Review
- Alveolar CCN1 is associated with mechanical stretch and acute respiratory distress syndrome severity.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Regulation of cellular senescence by extracellular matrix during chronic fibrotic diseases.Clinical science (London, England : 1979) · 2020Review
- The Roles of CCN1/CYR61 in Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Conjunction junction, what's the function? CCN proteins as targets in fibrosis and cancers.American journal of physiology. Cell physiology · 2020Review
- Dexamethasone and lenvatinib inhibit migration and invasion of non-small cell lung cancer by regulating EKR/AKT and VEGF signal pathways.Experimental and therapeutic medicine · 2020Article
- CCN1 expression by fibroblasts is required for bleomycin-induced skin fibrosis.Matrix biology plus · 2019Article
- Stretch-induced Expression of CYR61 Increases the Secretion of IL-8 in A549 Cells via the NF-κβ/lκβ Pathway.Current medical science · 2018Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Cysteine-rich protein-61 (CYR61), also known as connective tissue growth factor, CYR61, and nephroblastoma overexpressed gene 1 (CCN1), is a heparin-binding protein member of the CCN family of matricellular proteins. Gene expression profiles showed that Cyr61 is upregulated in human acute lung injury (ALI), but its functional role is unclear. We hypothesized that CYR61 contributes to ALI in mice. First, we demonstrated that CYR61 expression increases after bleomycin-induced lung injury. We then used adenovirus-mediated gene transfer to determine whether CYR61 overexpression in the lungs was sufficient to cause ALI. Mice instilled with CYR61 adenovirus showed greater weight loss, increased bronchoalveolar lavage total neutrophil counts, increased protein concentrations, and increased mortality compared with mice instilled with empty-vector adenovirus. Immunohistochemical studies in lungs from humans with idiopathic pulmonary fibrosis revealed CYR61 expression on the luminal membrane of alveolar epithelial cells in areas of injury. We conclude that CYR61 is upregulated in ALI and that CYR61 overexpression exacerbates ALI in mice.
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