Targeting The Pathophysiology And Therapy Of Liver Fibrosis
Funder
National Health and Medical Research Council
Funding Amount
$484,006.00
Summary
Hepatic fibrosis, or scarring of the liver, is a serious condition which can lead to liver cancer or death. Treatment of liver scarring is currently not effective once the scarring is well developed. This project aims to examine agents which may act to halt liver scarring once it has already developed. Outcomes from this project may help provide potential treatments to reduce the need for liver transplantation or to reduce patient deaths.
MERTK Receptor Tyrosine Kinase: A Novel Therapeutic Target For Liver Fibrosis
Funder
National Health and Medical Research Council
Funding Amount
$870,972.00
Summary
Hepatic fibrosis is the principal cause of liver-related morbidity and mortality, for which there are no effective therapies. Thus, there is an urgent and unmet need to identify new targets to treat liver fibrosis. We have demonstrated for the first time, that liver fibrosis correlates with elevated hepatic expression of MERTK, a receptor tyrosine kinase. This project will explore whether MERTK function can be exploited to target and reverse liver fibrosis
The Role Of The Hepatocyte And EMMPRIN In Liver Injury
Funder
National Health and Medical Research Council
Funding Amount
$607,487.00
Summary
This research plan investigates the role of the hepatocyte, the principal functional cell within the liver in the development of liver disease. Liver injury can result in end-stage scaring known as cirrhosis as well as leading to liver cancer. Our research aims to identify strategies for reversing the fibrotic process and result damage to the liver
The Role Of The Adiponectin Receptors In Liver Fibrosis
Funder
National Health and Medical Research Council
Funding Amount
$393,159.00
Summary
Advanced liver scarring (fibrosis) contributes to the death of 1500 Australians annually. Two-thirds of our community is overweight or obese, and this worsens liver disease. A protein secreted by fat, adiponectin, may be important as it acts on liver cells to promote fibrosis. To understand adiponectins role, we will use mice null for adiponectin receptor genes and study its action on liver cells. This study will improve our understanding of liver scarring biology and patient treatments.
Adiponectin And Cholesterol: A Driving Force In NASH Immunopathogenesis
Funder
National Health and Medical Research Council
Funding Amount
$436,017.00
Summary
This project examined the role of dietary cholesterol in the pathogenesis of fatty liver disease in a rodent model. We have been able to demonstrate that diets high in cholesterol lead to the development of inflammatory foci in the liver, elevations in the amount of hepatic ceramides (a lipid byproduct) and then leads to the activation of inflammatory molecular pathwways that lead to liver fibrosis. The latter results in end stage liver disease, and in some to the development of liver cancer.
THE ROLE OF THE HEPATOCYTE IN EXTRACELLULAR MATRIX INTERACTIONS IN LIVER FIBROGENESIS
Funder
National Health and Medical Research Council
Funding Amount
$540,438.00
Summary
This study focuses on the main cell within the liver, the hepatocyte, and its role in the development of liver fibrosis. Liver fibrosis arising from liver injury has a common progression characterised by loss of liver structure and the development of dense fibrous bands of tissue in the condition known as cirrhosis. The importance of the outlined research plan is that for the first time the hepatocyte has been identified as having a significant role in the development of liver fibrosis.
DPP4 Family Proteases As Drivers Of Chronic Liver Injury
Funder
National Health and Medical Research Council
Funding Amount
$730,041.00
Summary
Type 2 diabetes afflicts over 220 million people and often causes a chronic liver injury. That and hepatitis viruses can cause cirrhosis, liver failure and liver cancer, which is the 2nd most common cause of cancer death. Many Australians suffer from diabetes, fatty liver and/or hepatitis virus infection. We will understand these diseases far better and likely discover a new therapy by assessing roles of the DPP4 family of enzymes in diabetes, fibrosis and fatty liver.