Role of Matricellular CCN Proteins in Skeletal Muscle: Focus on CCN2/CTGF and Its Regulation by Vasoactive Peptides

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Abstract

The Cellular Communication Network (CCN) family of matricellular proteins comprises six proteins that share conserved structural features and play numerous biological roles. These proteins can interact with several receptors or soluble proteins, regulating cell signaling pathways in various tissues under physiological and pathological conditions. In the skeletal muscle of mammals, most of the six CCN family members are expressed during embryonic development or in adulthood. Their roles during the adult stage are related to the regulation of muscle mass and regeneration, maintaining vascularization, and the modulation of skeletal muscle fibrosis. This work reviews the CCNs proteins’ role in skeletal muscle physiology and disease, focusing on skeletal muscle fibrosis and its regulation by Connective Tissue Growth factor (CCN2/CTGF). Furthermore, we review evidence on the modulation of fibrosis and CCN2/CTGF by the renin-angiotensin system and the kallikrein-kinin system of vasoactive peptides.

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TGF-β: the master regulator of fibrosis.

Xiao-ming Meng, David J Nikolic-Paterson, Hui-Yao Lan (2016)

Transforming growth factor-β (TGF-β) is the primary factor that drives fibrosis in most, if not all, forms of chronic kidney disease (CKD). Inhibition of the TGF-β isoform, TGF-β1, or its downstream signalling pathways substantially limits renal fibrosis in a wide range of disease models whereas overexpression of TGF-β1 induces renal fibrosis. TGF-β1 can induce renal fibrosis via activation of both canonical (Smad-based) and non-canonical (non-Smad-based) signalling pathways, which result in activation of myofibroblasts, excessive production of extracellular matrix (ECM) and inhibition of ECM degradation. The role of Smad proteins in the regulation of fibrosis is complex, with competing profibrotic and antifibrotic actions (including in the regulation of mesenchymal transitioning), and with complex interplay between TGF-β/Smads and other signalling pathways. Studies over the past 5 years have identified additional mechanisms that regulate the action of TGF-β1/Smad signalling in fibrosis, including short and long noncoding RNA molecules and epigenetic modifications of DNA and histone proteins. Although direct targeting of TGF-β1 is unlikely to yield a viable antifibrotic therapy due to the involvement of TGF-β1 in other processes, greater understanding of the various pathways by which TGF-β1 controls fibrosis has identified alternative targets for the development of novel therapeutics to halt this most damaging process in CKD.

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Mechanisms of fibrosis: therapeutic translation for fibrotic disease.

Thomas Wynn, Thirumalai Ramalingam (2012)

Fibrosis is a pathological feature of most chronic inflammatory diseases. Fibrosis, or scarring, is defined by the accumulation of excess extracellular matrix components. If highly progressive, the fibrotic process eventually leads to organ malfunction and death. Fibrosis affects nearly every tissue in the body. Here we discuss how key components of the innate and adaptive immune response contribute to the pathogenesis of fibrosis. We also describe how cell-intrinsic changes in important structural cells can perpetuate the fibrotic response by regulating the differentiation, recruitment, proliferation and activation of extracellular matrix-producing myofibroblasts. Finally, we highlight some of the key mechanisms and pathways of fibrosis that are being targeted as potential therapies for a variety of important human diseases.

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Fibrosis--a common pathway to organ injury and failure.

Dan L Longo, Don C. Rockey, P Darwin Bell … (2015)

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Author and article information

Contributors

Kim S. Midwood: Role: Academic Editor

Kurt D. Hankenson: Role: Academic Editor

Olga Stenina Adognravi: Role: Academic Editor

Douglas Hamilton: Role: Academic Editor

Journal

Journal ID (nlm-ta): Int J Mol Sci

Journal ID (iso-abbrev): Int J Mol Sci

Journal ID (publisher-id): ijms

Title: International Journal of Molecular Sciences

Publisher: MDPI

ISSN (Electronic): 1422-0067

Publication date (Electronic): 15 May 2021

Publication date Collection: May 2021

Volume: 22

Issue: 10

Electronic Location Identifier: 5234

Affiliations

[1 ]Centro de Envejecimiento y Regeneración, CARE Chile UC, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile; mjose.acuna@ 123456ubo.cl

[2 ]Centro de Excelencia en Biomedicina de Magallanes (CEBIMA), Universidad de Magallanes, Punta Arenas 6213515, Chile

[3 ]Centro Integrativo de Biología y Química Aplicada (CIBQA), Universidad Bernardo O Higgins, Santiago 8370854, Chile

[4 ]Departamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile

[5 ]Fundación Ciencia & Vida, Santiago 7810000, Chile

Author notes

[* ]Correspondence: drebolledo@ 123456bio.puc.cl (D.L.R.); ebrandan@ 123456bio.puc.cl (E.B.); Tel.: +56-61-220-1413 (D.L.R.); +56-22-686-2725 (E.B.)

Author information

Daniela L. Rebolledo https://orcid.org/0000-0002-6240-6669

Article

Publisher ID: ijms-22-05234

DOI: 10.3390/ijms22105234

PMC ID: 8156781

SO-VID: b56eceb2-91aa-453e-88c4-7f2ef6ffaad0

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

Role of Matricellular CCN Proteins in Skeletal Muscle: Focus on CCN2/CTGF and Its Regulation by Vasoactive Peptides

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Most cited references 177

TGF-β: the master regulator of fibrosis.

Mechanisms of fibrosis: therapeutic translation for fibrotic disease.

Fibrosis--a common pathway to organ injury and failure.

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