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Updated: Jan 24, 2026

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
CREB family: A significant role in liver fibrosis
Guixin Li1, Qianqian Jiang1, Keshu Xu1
1Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Abstract:
Liver fibrosis (LF) is known as a result of the progressive accumulation of extracellular matrix (ECM), and always ascribed to chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, portal hypertension, and even multi-organ dysfunction and will bring up a health care burden worldwide. Cyclic AMP response-element binding protein (CREB), as a critical transcriptional factor, binds with conserved cAMP response-element (CRE), which is located in the promoter of targeted genes, to regulate the transcription. In the past decades, numerous studies have contributed to improved understanding of the links between CREB and liver fibrosis. In this review, we will summarize molecular mechanisms of CREB pathways and discuss contributions of CREB to liver fibrosis, focusing on activation and proliferation of hepatic stellate cells (HSCs), proliferation of cholangiocytes, deposition of extracellular matrix (ECM) and inflammation, for the development of antifibrotic therapies.
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