SYDNEY, June 14 (Xinhua) -- An international collaboration involving Australian and U.S. scientists, has announced a major breakthrough in the fight against chronic liver disease on Friday.
The University of Queensland (UQ) team in partnership with Cedars Sinai Medical Centre in the United States have identified a possible drug target for the debilitating and deadly illness.
According to researcher Dr. Divya Ramnath from UQ's Institute for Molecular Bioscience, a molecule called hyaluronan (HA), used as a marker for liver disease, also has a role in disease's progression.
"Testing for HA levels in the blood can indicate the severity of liver disease in patients, but until now its exact role in disease progression had not been completely understood," Ramnath said.
"Using clinical samples provided by Professor Elizabeth Powell from UQ's Faculty of Medicine, we were able to confirm that an enzyme which makes HA was at higher levels in patients with later stages of the disease," Ramnath said.
"This means it's not just a marker, it's now a potential drug target," Ramnath added.
According to Ramnath, with chronic liver disease now reaching "epidemic proportions", 30 percent of the world's population is now experiencing fat build up in the liver.
"Non-alcoholic fatty liver disease (NAFLD) can be slowed by changes in diet but if untreated constant liver damage and inflammation can lead to a condition associated with cirrhosis and liver cancer," she said.
"There are currently no medications to treat some forms of chronic liver disease so new drug targets are desperately needed," she said.
Because HA can create an immune response which causes inflammation, the molecule has been shown to increase the severity of the disease.
Now able to inhibit HA production in mice as part of the new study, researchers believe it's likely the severity of the disease can be reduced.
"This international collaboration has advanced our knowledge of this complex and prevalent disease, and the findings from this study may ultimately provide a strategy to develop much needed treatments," Professor Matt Sweet from UQ's Institute for Molecular Bioscience said.
