Harmeet Malhi, M.B.B.S., Â discusses current research efforts focusing on how and why the liver becomes injured in NASH. Dr. Malhi is Gastroenterology and Hepatology associate chair for research at Mayo Clinic in Rochester, Minnesota.
My name's Hermit Malhi. I am the associate chair for research for the division of gastroenterology and Hepatology. We really want to ask an answer fundamental mechanistic questions of how and why the liver is injured in Nash. One of these is to demonstrate that the toxicity of lipids are lipo toxicity leading to the cell death of hepatic sites is a key mediator of nash. A second set of observations pertains to examining how er stress activates what we call a Genova serra might synthesis pathway in the liver. This leads to the formation of these tiny tiny particles that sells release. We call them extra cellular vesicles. We've gone on to show that these E. V. S. That happen to sites are releasing as a consequence of er stress are pro inflammatory and they can attract macrophages into the liver. Print comma promoting liver inflammation. So one of the studies we've done has demonstrated that a lipid mediator, a molecule called fingers in one phosphate on these extra cellular vesicles communicates with immune cells through a set of receptors. And we can block this or the pharmacological inhibitor, a small molecule to show that we can improve nash. And our hope is to be able to identify the patients that say may benefit from inhibitors of the S one p. Or finger seen, one phosphate signaling pathway that our lab has identified. And we want to be able to treat nash at a time before patients develop advanced fibrosis or cirrhosis being visible in the field nationally and internationally. I'm able to attract phase three clinical trials to Mayo clinic for Nash patients, which are really necessary to be able to find the best drugs and targets for nash therapy.
