Michael P. Czech is currently the Isadore and Fannie Foxman Chair of Medical Research in the Program in Molecular Medicine at the University of Massachusetts Medical School. He was Chair of the Department of Biochemistry from 1981 to 1989, and was the founding Chair of the Program in Molecular Medicine (1989-2018). Czech earned the PhD degree in biochemistry in 1972 at Brown University under the mentorship of Professor John Fain, and completed postdoctoral study at Duke University Medical Center. He became Assistant Professor at Brown in 1974, rising to the rank of Professor in 1980. His research addresses mechanisms of signal transduction, metabolism and insulin resistance in type 2 diabetes and obesity. Czech’s laboratory has recently applied RNAi and CRISPR techniques to discover novel drug targets and to develop therapeutic strategies for alleviating inflammatory and metabolic diseases.
Czech has served on several editorial boards and NIH Study Sections and is a member of the Scientific Review Board of the Howard Hughes Medical Institute. He has received the Scientific Achievement Award (1982), the Banting Medal (2000) and the Albert Renold Award for mentorship (2004) from the American Diabetes Association; the David Rumbough Scientific Award of the Juvenile Diabetes Foundation (1985); NIH MERIT Awards (1997-2005 and 2012-2022); the Elliot P. Joslin Medal (1998), and the Jacobaeus Prize awarded in Umea, Sweden in 2009.
Czech Lab Research:
Gene editing and deletion to enhance insulin sensitivity in type 2 diabetes and obesity.
Major human diseases such as type 2 diabetes and atherosclerosis are promoted by dysfunctions in adipose tissue and in the interactions between adipocytes, endothelial cells, nerve fibers and immune cells. Adipose tissue remodeling in obesity can also secondarily disrupt liver and skeletal muscle metabolism, causing systemic insulin resistance and glucose intolerance. Our laboratory group is attacking key questions related to these cellular and molecular interactions among metabolic tissues, macrophages, neuronal signals and the vasculature that define both normal and metabolic disease states.
Central questions for our laboratory group are:
Can we identify molecular mechanisms that disrupt insulin signaling in obesity and type 2 diabetes to develop therapeutic strategies for these diseases?
Can we identify and modulate molecular mechanisms that switch adipocytes from storing triglyceride to cells that oxidize fat, expend energy and secrete beneficial factors?
Can we target genes that promote fatty liver and inflammation in obesity and diabetes with therapeutic siRNA to alleviate nonalcoholic steatohepatitis (NASH)?
Many of our projects take advantage of CRISPR and RNA interference (RNAi) to selectively silence normal or disease genes in vivo, providing both powerful research tools and potential approaches to therapies. Experiments in our laboratory are currently devoted to developing CRISPR- and siRNA-based delivery particles that can beneficially alter gene expression in adipocytes, hepatocytes and other cell types. Using these techniques, we have recently shown that gene editing of adipocytes by CRISPR can enhance their energy expenditure and fat oxidation. These efforts are advancing toward therapeutic applications.
Another approach that we have developed in collaboration with the Gary Ostroff laboratory is a method to deliver siRNA in vivo using glucan encapsulation vehicles (GeRPs). GeRPs can target macrophages in adipose tissue and liver to silence genes and attenuate tissue inflammation and insulin resistance.