Hui Tao, Jing-Jing Yang, Kai-Hu Shi, Cheng Huang, Lei Zhang, Xiong-Wen Lv, Jun Li
Objective: The aims of this review are to describe the present knowledge about YKL-40 protein, discuss its relation to liver fibrosis, and to look ahead at future perspectives of YKL-40 research.
Introduction: Liver fibrosis is characterized by excess collagen deposition, decreased extracellular matrix degradation and activation of hepatic stellate cells. Therefore, advancement in the identification of liver fibrosis biomarkers with diagnostic and prognostic values becomes an important tool for future molecular therapy. The molecular basis of YKL-40 in liver fibrosis is unknown.
Methods: A PubMed database search was performed for studies of YKL-40 in liver injury and fibrosis.
Results and conclusions: YKL-40 is an inflammatory glycoprotein involved in endothelial dysfunction by promoting chemotaxis, cell attachment and migration, reorganization, and tissue remodeling as a response to endothelial damage. Several studies demonstrate that elevated serum YKL-levels are independently associated with the presence of endothelial damage and even higher YKL-40 levels are documented in liver fibrosis. YKL-40 may play a key role in liver injury and fibrosis.