The Zhou laboratory studies factors and mechanisms that control heart and coronary vessel development to understand the pathogenesis of congenital heart disease and to gain insights into potential repairing mechanisms to combat both congenital and acquired heart diseases. Our research uses mice, mouse and human stem cells as model systems. We apply an integrated approach of genetics, developmental, molecular and systems biology as well as advanced single cell technologies and CRISPR gene editing to address three major questions: (1) How individual cardiac cells and lineages are specified, maintained, or diversified during heart and coronary vessel development, disease, aging or regeneration (Wu et al. Circ Res 2011, Wu et al. Cell 2012, Lu et al. Nat Commun 2022, Lu et al. Dev Cell 2023)? (2) How cell-cell, or cell-environment communications are modulated to control cardiac functions under these conditions (Wang et al. Eur Heart J 2015, Wang et al. Nat Commun 2017, Lu et al. Nat Cell Biol 2021)? (3) How fetal cardiac gene program is controlled during development and reactivated in the diseased or failing heart (Wang et al. Cardiovasc Res 2017, Lu et al. Circ Res 2022)?
University of Pennsylvania
Philadelphia
Fellowship - Heart Development
2002
University of Toronto
Toronto
PhD - Cardiovascular Pathobiology
1997
Nanjing Medical University
Nanjing
Fellowship - Cardiology
1991
Nanjing Medical University
Nanjing
Residency - Medicine
1989
Nanjing Medical University
Nanjing
MD - Medicine
1986
Epithelial-mesenchymal transition promotes metabolic reprogramming to suppress ferroptosis.
Epithelial-mesenchymal transition promotes metabolic reprogramming to suppress ferroptosis. Semin Cancer Biol. 2025 Jul; 112:20-35.
PMID: 40058616
L3MBTL3 and STAT3 collaboratively upregulate SNAIL expression to promote metastasis in female breast cancer.
L3MBTL3 and STAT3 collaboratively upregulate SNAIL expression to promote metastasis in female breast cancer. Nat Commun. 2025 01 02; 16(1):231.
PMID: 39747894
NF-?B represses retinoic acid receptor-mediated GPRC5A transactivation in lung epithelial cells to promote neoplasia.
NF-?B represses retinoic acid receptor-mediated GPRC5A transactivation in lung epithelial cells to promote neoplasia. JCI Insight. 2024 10 08; 9(19).
PMID: 39377225
Correction: Nac1 promotes stemness and regulates myeloid-derived cell status in triple-negative breast cancer.
Correction: Nac1 promotes stemness and regulates myeloid-derived cell status in triple-negative breast cancer. Mol Cancer. 2024 Oct 03; 23(1):220.
PMID: 39358788
NAC1 promotes stemness and regulates myeloid-derived cell status in triple-negative breast cancer.
NAC1 promotes stemness and regulates myeloid-derived cell status in triple-negative breast cancer. Mol Cancer. 2024 Sep 06; 23(1):188.
PMID: 39243032
Epigenetic repression of Cend1 by lysine-specific demethylase 1 is essential for murine heart development.
Epigenetic repression of Cend1 by lysine-specific demethylase 1 is essential for murine heart development. iScience. 2024 Jan 19; 27(1):108722.
PMID: 38226173
A sandwiched ventricular explant assay to model mouse coronary angiogenesis ex vivo.
A sandwiched ventricular explant assay to model mouse coronary angiogenesis ex vivo. STAR Protoc. 2023 12 15; 4(4):102619.
PMID: 37897735
Crk and Crkl Are Required in the Endocardial Lineage for Heart Valve Development.
Crk and Crkl Are Required in the Endocardial Lineage for Heart Valve Development. J Am Heart Assoc. 2023 09 19; 12(18):e029683.
PMID: 37702066
PROX1 Inhibits PDGF-B Expression to Prevent Myxomatous Degeneration of Heart Valves.
PROX1 Inhibits PDGF-B Expression to Prevent Myxomatous Degeneration of Heart Valves. Circ Res. 2023 09; 133(6):463-480.
PMID: 37555328
ß-Catenin regulates endocardial cushion growth by suppressing p21.
ß-Catenin regulates endocardial cushion growth by suppressing p21. Life Sci Alliance. 2023 09; 6(9).
PMID: 37385754
Fellow of the American Heart Association
American Heart Association
2011