Canadian Institutes of Health Research Group in Skeletal Development and Remodeling, Division of Oral Biology and Department of Physiology and Pharmacology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON, N6A 5C1, Canada,
J Cell Commun Signal. 2009 Jun;3(2):161-2. doi: 10.1007/s12079-009-0056-4. Epub 2009 May 29.
Fibrotic disease is a significant cause of mortality. CCN2 (connective tissue growth factor [CTGF]), a member of the CCN family of matricellular proteins, plays a significant role in driving the fibrogenic effects of cytokines such as transforming growth factor beta (TGFbeta). It has been proposed that other members of the CCN family can either promote or antagonize the action of CCN2, depending on the context. A recent elegant study published by Bruce Riser and colleagues (Am J Pathol. 174:1725-34, 2009) illustrates that CCN3 (nov) antagonizes the fibrogenic effects of CCN2. This paper, the subject of this commentary, raises the intriguing possibility that CCN3 may be used as a novel anti-fibrotic therapy.
纤维化疾病是导致死亡的一个重要原因。CCN2（结缔组织生长因子[CTGF]）是细胞外基质蛋白家族的一员，在驱动细胞因子如转化生长因子-β（TGF-β）的纤维生成作用方面起着重要作用。据认为，细胞外基质蛋白家族的其他成员可以根据具体情况促进或拮抗 CCN2 的作用。Bruce Riser 及其同事最近发表的一项精彩研究（Am J Pathol. 174:1725-34, 2009）表明 CCN3（nov）拮抗 CCN2 的纤维生成作用。本文讨论了这一可能性，即 CCN3 可能被用作一种新型的抗纤维化治疗方法。
