Haodi Wu, PhD
Assistant Professor of Medicine, Division of Cardiology
Dr. Haodi Wu is an assistant professor in the Vascular Medicine Institute, Department of Medicine at the University of Pittsburgh. He received his PhD from Peking University in China, where he studied the regulatory role of miRNA and JPH2 in the morphological and functional remodeling of heart failure. After graduation, he continued his research in Dr. Joseph Wu’s lab as a postdoctoral fellow in the Cardiovascular Institute, Stanford University to understand the pathogenesis of familial cardiomyopathies. His research has revealed the novel epigenetic regulation during DCM pathogenesis and the mechanism of impaired calcium homeostasis in HCM patients with diastolic dysfunction. During his postdoctoral training, he was funded by multiple mechanisms including American Heart Association postdoctoral fellowship, NIH PCBC Jump Start Award, and NIH K99 pathway to independence Award. The main research interest of Dr. Haodi Wu’s lab at U Pitt is to combine cutting-edge stem cell, physiology, genetics, and molecular approaches to dissect the mechanisms of cardiac dysfunction related to mutation, aging, and environmental risk factors, and ultimately, to develop novel strategies to target these pathological remodeling.
Heart diseases remain the leading cause of death for men, women, and people of most racial and ethnic groups worldwide. The top risk factors for heart disease include familial history (genetic mutations), aging, unhealthy lifestyle (smoking, alcohol addition, high fat diet etc.), obesity, etc. However, the studies of the pathological mechanisms of these risk factors in the human heart was greatly humbled by the lack of standardized research models, as human cardiac cells are limited resources, and genetically modified animals show significant species variations. As a result of our incomplete understanding of pathological mechanisms, the current treatment of heart disease mostly focuses on relieving symptoms, rather than targeting the underlying molecular basis.
Human induced pluripotent stem cells (iPSCs) have provided us an exceptional research platform for the mechanistic studies of cardiac diseases in human originated cardiac cells. The researches at Wu lab take advantage of modern stem cell, physiology, genome-editing, and omics technologies to 1) Dissect the molecular mechanisms of inherited dilated and hypertrophic cardiomyopathies; 2) Understand the molecular mechanism of aging in heart cells; 3) Study how environmental risk factors contribute to the remodeling of cardiomyocyte. The long-term goal of our research is to gain a deep mechanistic understanding of the pathogenesis in diseased cardiac cells, and to develop novel molecular tools and compounds to rectify the regulation during the process.
Induced pluripotent stem cell model, Inherited cardiomyopathies, Calcium handling, Genome editing, Cardiac arrhythmias, Cardiac aging, Heart failure
Education and Training
Postdoctoral Fellow, Stanford University
Instructor, Stanford University
For a complete bibliography, click here.
View Recent Papers
- Yang H, Shao N, Holmström A, Zhao X, Chour T, Chen H, Itzhaki I, Wu H, Ameen M, Cunningham NJ, Tu C, Zhao MT, Tarantal AF, Abilez OJ, Wu JC. Transcriptome Analysis of Non-Human Primate Induced Pluripotent Stem Cell-Derived Cardiomyocytes in 2D Monolayer Culture versus 3D Engineered Heart Tissue. Cardiovasc Res. 2020. [Epub ahead of print] PubMed PMID: 33002105.
- Li LL, Guo QJ, Lou HY, Liang JH, Yang Y, Xing X, Li HT, Han J, Shen S, Li H, Ye H, Di Wu H, Cui B, Wang SQ. Nanobar Array Assay Revealed Complementary Roles of BIN1 Splice Isoforms in Cardiac T-Tubule Morphogenesis. Nano Lett. 2020. PubMed PMID: 32787151.
- Liu Q*, Wu H*, Luo QJ, Jiang C, Duren Z, Bortle KV, Zhao MT, Zhao B, Liu J, Marciano DP, Lee-McMullen B, Zhu C, Narasimha AM, Gruber JJ, Lipchik AM, Guo H, Watson NK, Tsai MS, Furihata T, Tian L, Wei E, Li Y, Steinmetz LM, Wong WH, Kay MA, Wu JC, Snyder MP. Tyrosine Kinase Inhibitors Induce Mitochondrial Dysfunction During Cardiomyocyte Differentiation Through Alteration of GATA4-Mediated Networks. BioRxiv. 2020.
- Buikema JW, Lee S, Goodyer WR, Maas RG, Chirikian O, Li G, Miao Y, Paige SL, Lee D, Wu H, Paik DT, Rhee S, Tian L, Galdos FX, Puluca N, Beyersdorf B, Hu J, Beck A, Venkamatran S, Swami S, Wijnker P, Schuldt M, Dorsch LM, van Mil A, Red-Horse K, Wu JY, Geisen C, Hesse M, Serpooshan V, Jovinge S, Fleischmann BK, Doevendans PA, van der Velden J, Garcia KC, Wu JC, Sluijter JPG, Wu SM. Wnt Activation and Reduced Cell-Cell Contact Synergistically Induce Massive Expansion of Functional Human iPSC-Derived Cardiomyocytes. Cell Stem Cell. 2020. PubMed PMID: 32619518; PubMed Central PMCID: PMC7334437.