Formerly known as nonalcoholic steatohepatitis, metabolic dysfunction-associated steatohepatitis (MASH) is an inflammatory disease characterized by liver scarring or fibrosis that progressively impairs liver function. It is a major risk factor for cirrhosis and liver cancer. And because treatment options are limited, MASH is the second leading cause of liver transplants in the United States after cirrhosis caused by chronic hepatitis C infection.
A better understanding of the pathological processes that drive MASH is critical to creating effective treatments. In a new paper published in Proceedings of the National Academy of Sciences, a team of scientists from Sanford Burnham Prebys, the University of California San Diego School of Medicine and elsewhere describes the complex interplay between diseased liver cells and macrophages—a type of white blood cell whose jobs include killing and removing harmful cells and pathogens and helping to spur normal healing. Debanjan Dhar, Ph.
D., associate professor in the Cancer Genome and Epigenetics Program at Sanford Burnham Prebys, is senior author of the study. David Brenner, MD, president and CEO of Sanford Burnham Prebys, and Christopher Glass, MD, Ph.
D., professor of cellular and molecular medicine at UC San Diego, are corresponding authors. Souradipta Ganguly, Ph.
D., a postdoctoral research fellow at UC San Diego and Sanford Burnham Prebys, is the first author. The researchers found that the heterogeneous mix of macrophages involv.