I trained as a developmental biologist. My initial interest was to understand liver development by looking at how different cell types are specified and brought together to form a complex organ. At Cincinnati Children's Hospital Medical Center, I work with physicians treating patients with liver problems. I feel that my expertise and skills contribute to the study of liver disease mechanisms so that we can save more lives.
My current work focuses on hepatocytes and cholangiocytes. Using transgenic zebrafish marking these cell types along with related reagents, I study their cellular behavior and function in liver development, disease and underlying molecular regulations.
I developed a novel zebrafish model to study the disease caused by a deficiency in the bile salt export pump transporter. Using this model, I discovered new strategies for patient treatment. Through collaborative work with a physician, my colleagues and I also discovered a new gene associated with childhood chronic cholestatic liver disease.
I used to spend all my time in the lab because science is what interested me the most. In 2019, at a family conference co-hosted by Cincinnati Children’s, I had the opportunity to meet the patients with the rare liver disease that I am studying and their families. They came from all over the world. Being able to introduce my research to them and show them the progress we are making is exciting to me. Seeing the devastation of the disease firsthand motivates me in my work. I am thankful to Cincinnati Children’s for providing me with the opportunity to interact with patients and make my job even more rewarding.
My lab is funded by an R01 grant from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and the Center for Autoimmune Liver Disease at Cincinnati Children’s Hospital Medical Center. I have received a pilot feasibility award from the American Gastroenterological Association (AGA).
BS: Evolution and Ecology, Fudan University, Shanghai, China, 2001.
PhD: Developmental Biology, Vanderbilt University, Nashville, TN, 2007.
Postdoctoral fellow: Developmental Biology, University of California at San Francisco, San Francisco, CA, 2012.
Liver biology; cholestasis; molecular genetics of pediatric liver diseases
Gastroenterology Hepatology and Nutrition, Developmental Biology
A missense mutation in the proprotein convertase gene furinb causes hepatic cystogenesis during liver development in zebrafish. Hepatology Communications. 2022; 6:3083-3097.
Deleterious Variants in ABCC12 are Detected in Idiopathic Chronic Cholestasis and Cause Intrahepatic Bile Duct Loss in Model Organisms. Gastroenterology. 2021; 161:287-300.e16.
Macrophages in Zebrafish Models of Liver Diseases. Frontiers in Immunology. 2019; 10.
Mannose Phosphate Isomerase and Mannose Regulate Hepatic Stellate Cell Activation and Fibrosis in Zebrafish and Humans. Hepatology. 2019; 70:2107-2122.
Zebrafish as a Model to Study Cholestatic Liver Diseases. Methods in Molecular Biology. 2019; 1981:273-289.
Gon4l regulates notochord boundary formation and cell polarity underlying axis extension by repressing adhesion genes. Nature Communications. 2018; 9.
Chunyue Yin, PhD, William F. Balistreri, MD ...12/6/2021
Chunyue Yin, PhD, Alexander G. Miethke, MD3/23/2021