Emerging role of CCN family proteins in fibrosis. Issue 6 (22nd November 2020)

• Record Type: Journal Article
• Authors: Sun, Chao; Zhang, Han; Liu, Xinhui
• Is Part Of: Journal of cellular physiology. Volume 236:Issue 6(2021)
• Page Start: 4195
• Page End: 4206
• Publication Date: 2020-11-22
• Subjects: CCN protein -- extracellular matrix -- fibrosis -- myofibroblasts -- TGF‐β; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.30171
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: Fibrosis is a common pathological change characterized by the excessive accumulation of fibrous connective tissue. Once uncontrolled, this pathological progress can lead to irreversible damage to the structure and function of organs, which is a serious threat to human health and life. Actually, the disability and death of patients caused by many chronic diseases have a closed relationship with fibrosis. The CCN protein family, including six members, is a small group of matrix proteins exhibiting structurally similar features. In the past 20 years, different biological functions of CCN proteins have been identified in various diseases. Of note, it has been recently shown that they are implicated in the key pathological process of fibrosis. In this review, we summarize the current status of knowledge regarding the role of CCN proteins involved in the pathogenesis of fibrosis diseases in detail. Furthermore, we highlight some of the underlying interaction mechanisms of CCN protein acting in fibrosis that helps to develop new drugs and determine appropriate clinical strategies for fibrotic diseases. Abstract : During the fibrosis process, the composition, form, and functionality of extracellular matrix (ECM) undergo a dramatic restructuring. CCN family proteins involve in ECM remodeling and regulate fibrosis of multiple tissues and organs including the heart, kidney, lung, liver, and skin. We will critically focus on the key role of the six CCN family members in various fibrosis disease processes.