I come from northwestern China. I obtained my B.S. in Biological Science from Henan University and got my M.S. in Cell Biology from Emporia State University. I joined the IGPBS program at The University of Kansas Medical Center in 2017 and joined Dr. Ding’s Lab in July of 2018.
Alcohol-related liver disease (ALD) is a worldwide health problem without successful treatment. Aging is associated with obesity, which is known as a risk factor that aggravates ALD. Our lab and others have previously demonstrated that chronic plus binge alcohol increases adipose tissue lipolysis and promotes alcohol-induced liver injury through the adipose-liver crosstalk. One of my projects is investigating the role of autophagy receptor protein SQSTM1/p62 in adipose-liver crosstalk and the effects of aging and obesity in ALD.
p62 also is a stress-inducible cellular protein that can bind to various partners through its multiple domains which are involved in various signaling pathways. p62 is a common component of many human disease-related cellular inclusion bodies, especially Mallory-Denk bodies (MDBs), intracytoplasmic hyaline bodies (IHBs), and α1 antitrypsin aggregates in the liver. The existence of p62 related aggregates, such as MDBs, in hepatocytes, is an indicator of liver damage and a hallmark of alcoholic liver disease, however, the function and mechanism of p62 in the formation of p62 related aggregates are still unknown. I would also like to address the role of p62 mediated aggregates in alcohol-induced liver injury.