About
Biography
As many as one in 100 children face cardiovascular problems, such as heart chamber defect or valvular underdevelopment. These heart problems often develop in the first few days or weeks after birth.
I’ve been interested in cardiovascular disease investigations since I was a student in medical school. My research interests include congenital heart defect and vasculature disease. I also study pulmonary arterial hypertension and other congenital pulmonary diseases.
In my research lab, my team and I attempt to identify the vasculature irregularities in congenital diseases, including single ventricle disease, valve disease and pulmonary hypertension. We do this by generating multiple cardiac cell types and organoids from patient-specific induced pluripotent stem cells (iPSCs).
One of my notable discoveries includes a novel long non-coding RNA, LEENE, that controls the homeostasis of endothelial cells via chromatin remodeling. In the early years of my research, I demonstrated how nuclear receptors contribute to brown adipocyte metabolism and energy expenditure. I’ve also recently discovered endocardial dysfunctions underlying hypoplastic left heart syndrome through iPSCs platform and single cell sequencing technology.
I have more than ten years of experience in the cardiovascular research field and joined the team at Division of Neonatology and CuSTOM stem cell research center at Cincinnati Children’s Hospital Medical Center in 2020. My research has been published in prestigious journals, such as Cell Stem Cell, Circulation, Nature Communications, and Proceedings of the National Academy of Sciences of the United States of America.
MBBS: Peking University Health Science Center, Beijing, China, 2008.
PhD: Peking University Health Science Center, Beijing, China, 2012.
Research Fellow: University of Houston, Houston, TX, 2016.
Research Fellow: City of Hope National Medical Center, Duarte, CA, 2018.
Research Associate: Stanford University School of Medicine, Stanford, CA, 2020.
Interests
Organoids; human pluripotent stem cell; congenital cardiac and pulmonary defect; single ventricle defects; epigenetic regulation
Research Areas
Neonatology, Perinatal Biology, Pulmonary Biology
Publications
KMT2D-NOTCH Mediates Coronary Abnormalities in Hypoplastic Left Heart Syndrome. Circulation Research. 2022; 131:280-282.
Remodeling of active endothelial enhancers is associated with aberrant gene-regulatory networks in pulmonary arterial hypertension. Nature Communications. 2020; 11:1673.
Intrinsic Endocardial Defects Contribute to Hypoplastic Left Heart Syndrome. Cell Stem Cell. 2020; 27:574-589.e8.
Suppression of Endothelial AGO1 Promotes Adipose Tissue Browning and Improves Metabolic Dysfunction. Circulation. 2020; 142:365-379.
Isolation of Endocardial and Coronary Endothelial Cells from the Ventricular Free Wall of the Rat Heart. Jove-Journal of Visualized Experiments. 2020; 2020.
Enhancer-associated long non-coding RNA LEENE regulates endothelial nitric oxide synthase and endothelial function. Nature Communications. 2018; 9:292.
An ERβ agonist induces browning of subcutaneous abdominal fat pad in obese female mice. Scientific Reports. 2016; 6:38579.
Prostaglandin E2 receptor EP3 regulates both adipogenesis and lipolysis in mouse white adipose tissue. Journal of Molecular Cell Biology. 2016; 8:518-529.
Liver X receptor β controls thyroid hormone feedback in the brain and regulates browning of subcutaneous white adipose tissue. Proceedings of the National Academy of Sciences of USA. 2015; 112:14006-14011.
Inactivation of the E-prostanoid 3 receptor attenuates the angiotensin II pressor response via decreasing arterial contractility. Arteriosclerosis, Thrombosis, and Vascular Biology. 2012; 32:3024-3032.
From the Blog
New ‘Atlas’ of Human Heart Valve Development May Guide Next-Gen Therapies
Yifei Miao, MBBS, PhD, Mingxia Gu, MD, PhD7/29/2024
3333 Burnet Avenue, Cincinnati, Ohio 45229-3026
© 1999-2024 Cincinnati Children's Hospital Medical Center. All rights reserved.
