New Leads in the Development and Treatment of Liver Disease
Researchers unravel processes behind alcohol-induced liver damage, acetaminophen overdose, cirrhosis and liver cancer
Newswise — A treatment gap remains for many conditions involving damage to the liver, the body’s main organ for removing toxins, among other functions. The Experimental Biology 2018 meeting (EB 2018) will feature important research announcements related to the causes of liver degradation and possible treatments.
Receptor for sleep hormone melatonin may play a role in liver cirrhosis
Texas A&M University College of Medicine and Central Texas Veterans Health Care System researchers have discovered a potential new lead for treating chronic liver diseases. The research focuses on melatonin, a hormone associated with maintaining circadian rhythms. Receptors for this hormone can be found in the liver, as well as elsewhere in the body, and previous experiments using mice have shown that melatonin helps reduce the processes that cause liver fibrosis (scarring that ultimately leads to cirrhosis). When the researchers bred mice that were incapable of expressing different kinds of melatonin receptors, the mice showed different rates of liver fibrosis. Fibrosis was significantly decreased in mice incapable of expressing one receptor in particular, known as MT1. This suggests that drugs designed to block MT1 activity could potentially help slow liver disease progression.
Nan Wu will present this research at the American Society for Investigative Pathology annual meeting at EB on Saturday, April 21, from 8:35–8:45 a.m. in Room 2 (abstract) and on Tuesday, April 24, from 4:15–4:30 p.m. in Room 5A.
Deciphering the links between alcoholism and liver cancer
Steatohepatitis is a type of fatty liver disease that can lead to cirrhosis and liver cancer. While it can occur in people who drink little or no alcohol, it is far more common—and more likely to progress to liver cancer—in people with alcoholism. A new study by researchers at Harbor–UCLA Medical Center reveals how the expression of certain proteins in the liver differs between patients with non-alcoholic steatohepatitis and alcoholic steatohepatitis. The researchers investigated 10 proteins that are known to play a role in cancer development. Both patient groups showed increased levels of most of the proteins compared to healthy people, but the protein levels were much higher in those with alcoholic steatohepatitis, which helps explain why these patients face such a high risk of liver cancer.
Jiajie Lu will present this research at the American Society for Investigative Pathology annual meeting at EB on Sunday, April 22, from 11:45 a.m.–12:45 p.m. in the Exhibit Hall (poster D31) (abstract) and on Tuesday, April 24, from 5:30–7:30 p.m. in Ballroom 20BC.
Potential therapeutic target for liver damage from acetaminophen
Taking too much acetaminophen (the active ingredient in Tylenol®) can cause serious liver damage and even death. In a new study, researchers at the Central Texas Veterans Health Care System and Texas A&M University Health Science Center identify a possible new way to interfere with the process by which acetaminophen damages liver cells. The research focuses on the role a protein, transforming growth factor beta 1 (TGFβ1), plays in the cascade of events that leads to cell death. Scientists discovered that the damage caused by acetaminophen was reversed in mice bred without the ability to produce TGFβ1 and in genetically normal mice that were treated with a TGFβ1-disabling agent. The results suggest that interrupting TGFβ1’s activity could be one way to prevent or treat acetaminophen-related liver injury. This work was supported by Central Texas Veterans Health Care System and Texas A&M University Health Science Center, Temple, Texas.
Matthew McMillin will present this research at the American Society for Investigative Pathology annual meeting at EB on Tuesday, April 24, from 2:15–2:30 p.m. in Room 5A (abstract) and on Tuesday, April 24 from 5:30–7:30 p.m. in Ballroom 20BC (poster 415.2).
New insights on non-coding RNA in alcoholic liver disease
A tiny segment of RNA known as microRNA-21 has been found to play a role in cancer and heart disease. New research from the University of Connecticut suggests the molecule also influences the processes involved in alcoholic liver disease, a leading cause of cirrhosis. While microRNA-21 does not itself code for cellular functions the way DNA does, it can interfere with how other genes are expressed. In the study, mice fed a diet spiked with alcohol produced significantly higher amounts of microRNA-21 in the liver compared to mice on a normal diet. Tissue samples from human volunteers also found microRNA-21 levels were markedly increased in people with alcohol-related cirrhosis compared to healthy individuals. The researchers gained additional insights about the ways microRNA-21 affects liver health by breeding mice that were incapable of producing microRNA-21 in their livers.
Yulan Zhao will present this research at the American Society for Investigative Pathology annual meeting at EB on Sunday, April 22, from 4:15–5:15 p.m. in Room 4 (abstract) and on Tuesday, April 24, from 5:30–7:30 p.m. in Ballrooms 20BC (poster 150.10).
EB 2018 is the premier annual meeting of five scientific societies to be held April 21–25 at the San Diego Convention Center. Contact the media team for abstracts, images and interviews, or to obtain a free press pass to attend the meeting.
About Experimental Biology 2018
Experimental Biology is an annual meeting that attracts more than 14,000 scientists and exhibitors from five host societies and more than two dozen guest societies. With a mission to share the newest scientific concepts and research findings shaping clinical advances, the meeting offers an unparalleled opportunity for exchange among scientists from across the U.S. and the world who represent dozens of scientific areas, from laboratory to translational to clinical research. www.experimentalbiology.org #expbio
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