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The advance of CCN3 in fibrosis

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Journal of Cell Communication and Signaling Aims and scope

Abstract

The extracellular matrix (ECM) is comprised of various extracellular macromolecules, including collagen, enzymes, and glycoproteins, which offer structural and biochemical support to neighboring cells. After tissue injury, extracellular matrix proteins deposit in the damaged tissue to promote tissue healing. However, an imbalance between ECM production and degradation can result in excessive deposition, leading to fibrosis and subsequent organ dysfunction. Acting as a regulatory protein within the extracellular matrix, CCN3 plays a crucial role in numerous biological processes, such as cell proliferation, angiogenesis, tumorigenesis, and wound healing. Many studies have demonstrated that CCN3 can reduce the production of ECM in tissues through diverse mechanisms thereby exerting an inhibitory effect on fibrosis. Consequently, CCN3 emerges as a promising therapeutic target for ameliorating fibrosis.

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Funding

This work was supported by the National Natural Science Foundation of China (82260112, 81960296), Jiangxi Provincial Natural Science Foundation (20202ACBL206011), Jiangxi Provincial Clinical Research Center for Rheumatic and Immunologic Diseases (20192BCD42005), Jiangxi Province Medical Leading Discipline Construction Project (Rheumatology), and Provincial and municipal joint construction projects of medical disciplines in Jiangxi Province (Rheumatology).

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HY and NL reviewed the literature and wrote the first draft. HY, NL, and LD reviewed the literature and finalized the manuscript. HY, XZ, and LD revised the manuscript. All authors have read and approved the final manuscript.

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Correspondence to Lihua Duan.

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Yin, H., Liu, N., Zhou, X. et al. The advance of CCN3 in fibrosis. J. Cell Commun. Signal. 17, 1219–1227 (2023). https://doi.org/10.1007/s12079-023-00778-3

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