ArticleJournal of cell communication and signaling2022
Tissue distribution and transcriptional regulation of CCN5 in the heart after myocardial infarction.
Article in Journal of cell communication and signaling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Beyond cardiac fibroblasts: research advances on understanding and targeting intercellular communication networks in cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- A panel of plasma proteins associated with venous thromboembolism in patients with prostate cancer.Cancer biomarkers : section A of Disease markers · 2025Article
- Adipocyte death promotes hepatic infiltration of S100A8+ macrophages and steatotic liver disease progression in mice.The Journal of clinical investigation · 2025Article
- CCN5 negatively regulates TGF-β-induced endometriosis associated fibrosis through Wnt/β-catenin signaling via Smad3-dependent mechanism.Journal of translational medicine · 2025Article
- CCN5/WISP2 serum levels in patients with coronary artery disease and type 2 diabetes and its correlation with inflammation and insulin resistance; a machine learning approach.Biochemistry and biophysics reports · 2024Article
- CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023Review
- Modeling the microenvironment special issue.Journal of cell communication and signaling · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
CCN5 is a divergent member of the cellular communication network factor (CCN) family in that it lacks the carboxyl terminal cystine knot domain common to the other CCN family members. CCN5 has been reported to antagonize the profibrotic actions of CCN2 and to inhibit myocardial collagen deposition and fibrosis in chronic pressure overload of the heart. However, what mechanisms that regulate CCN5 activity in the heart remain unknown. Recombinant, replication defective adenovirus encoding firefly luciferase under control of the human CCN5 promoter was prepared and used to investigate what mechanisms regulate CCN5 transcription in relevant cells. Tissue distribution of CCN5 in hearts from healthy mice and from mice subjected to myocardial infarction was investigated. Contrary to the profibrotic immediate early gene CCN2, we find that CCN5 is induced in the late proliferation and maturation phases of scar healing. CCN5 was identified principally in endothelial cells, fibroblasts, smooth muscle cells, and macrophages. Our data show that CCN5 gene transcription and protein levels are induced by catecholamines via β
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