Adiponectin and its role in wound healing


This project will use mouse models to investigate the role of adiponectin and its receptors in liver fibrosis.


Dr Lionel Hebbard

Research Location

Westmead - Westmead Institute for Medical Research

Program Type



Over 1500 Australians succumb to end stage chronic liver disease each year. The pathological substrate for this is the development of progressive fibrosis leading to cirrhosis. The hepatic wound healing response, of which fibrosis is a consequence, is orchestrated at the cellular level by numerous factors including reactive oxygen species (ROS), hormones, cytokines and the extracellular matrix (ECM). In this context, fatty liver disease is emerging as a major cause of liver disease and recent research has focussed on the role of adipose secreted cytokines (adipokines) such as adiponectin and leptin in the modulation of liver injury and fibrosis. Low adiponectin is an established risk factor for the development of fatty liver disease. In the liver, hypoadiponectinemia is associated with steatosis, inflammation and fibrosis, while the converse holds true when levels are normal. However, the precise molecular mechanisms by which adiponectin modulates liver injury and fibrosis have not been characterized. Hence, the overall aim of this project is to understand the mechanisms by which adiponectin is protective against the development of liver inflammation and fibrosis, with particular reference to its effects on hepatic non parenchymal cells that are critical to this process. Techniques used in this project: * Mouse models, primary cell isolation. * Histology, confocal microscopy. * PCR, gene cloning. * Recombinant protein expression. * Adenovirus/lentivirus generation. * Protein analysis (SDS-PAGE, Western Blotting). * In vitro assays of primary liver non-parenchymal cells.

Additional Information

The Storr Liver Unit

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Liver fibrosis, fatty liver, fatty liver disease, signaling, Mouse models, adiponectin

Opportunity ID

The opportunity ID for this research opportunity is: 861

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