Open AccessEt tu, CCN1….
Author(s) -
Leask Andrew
Publication year - 2020
Publication title -
journal of cell communication and signaling
Language(s) - French
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-020-00573-4
Subject(s) - cyr61 , ctgf , matricellular protein , steatohepatitis , fibrosis , transforming growth factor , cancer research , growth factor , mechanotransduction , medicine , biology , microbiology and biotechnology , pathology , disease , extracellular matrix , fatty liver , receptor
The CCN family of matricellular proteins are recognized bona fide targets for therapeutically targeting so‐called chronic inflammatory diseases, including fibrosis and cancers. The majority of the work supporting this contention has been derived from examining CCN2, formerly, and unhelpfully, termed “connective tissue growth factor.” Both CCN2, and its related protein, CCN1, formerly termed “cysteine‐rich protein 61”, are positively regulated by not only TGFbeta, but also by the hippo/YAP/TAZ mechanotransduction pathway that appears to drive these pathologies. Indeed, increasing evidence indicates that CCN1 also contributes to these fibrosis and cancers and, consequently, targeting both CCN2 and CCN1 simultaneously could be of therapeutic value. This commentary focuses on a recent, exciting paper (Ju et al., 2020, Scientific Reports , 10 , 3201) suggesting that CCN1 is a target for non‐alcoholic steatohepatitis (NASH).