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Archive - Jan 16, 2012

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Gap-Junction Inhibitors May Prevent Drug-Induced Liver Damage

Rutgers University and Massachusetts General Hospital (MGH) investigators have developed a novel strategy to protect the liver from drug-induced injury and improve associated drug safety. In a report published online on January 15, 2012 in the journal Nature Biotechnology, the team reports that inhibiting a type of cell-to-cell communication can protect against damage caused by liver-toxic drugs such as acetaminophen. "Our findings suggest that this therapy could be a clinically viable strategy for treating patients with drug-induced liver injury," said Dr. Suraj Patel a postdoctoral researcher in the Center for Engineering in Medicine at MGH and the paper's lead author. "This work also has the potential to change the way drugs are developed and formulated, which could improve drug safety by providing medications with reduced risk of liver toxicity." Drug-induced liver injury is the most common cause of acute liver failure in the U.S. and is also the most frequent reason for abandoning drugs early in development or withdrawing them from the market. Liver toxicity limits the development of many therapeutic compounds and presents major challenges to both clinical medicine and to the pharmaceutical industry. Because no pharmaceutical strategies currently exist for preventing drug-induced liver injury, treatment options are limited to discontinuing the offending drug, supportive care, and transplantation for end-stage liver failure. The researchers investigated an approach that targets a liver's gap junctions – hollow multimolecular channels that connect neighboring cells and allow direct communication between coupled cells. In the heart, gap junctions propagate the electrical activity required for synchronized contraction, but their role in the liver has not been well understood.