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Career

· Doctor of Medicine, Capital Medical University2018–2021
· Research Assistant, Capital Medical University2010–
· Researcher Associate, China Rehabilitation Research Center2010–
· Master's degree, Central Conservatory of Music2006–2009
· Bachelor's degree, Yantai Normal University2000–2004

Publications (140)

Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure.
Journal of Clinical Investigation · 2007
423
cited
Ca2+ Influx–Induced Sarcoplasmic Reticulum Ca2+ Overload Causes Mitochondrial-Dependent Apoptosis in Ventricular Myocytes
Circulation Research · 2005
219
cited
GDF11 does not rescue aging-related pathological hypertrophy.
Circulation Research · 2015
178
cited
Cardiotoxic and Cardioprotective Features of Chronic &bgr;-Adrenergic Signaling
Circulation Research · 2013
129
cited
Adolescent Feline Heart Contains a Population of Small, Proliferative Ventricular Myocytes With Immature Physiological Properties
Circulation Research · 2007
127
cited
Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.
Journal of Molecular and Cellular Cardiology · 2011
113
cited
Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress
Proceedings of the National Academy of Sciences of the United States of America · 2014
90
cited
Phosphodiesterases coordinate cAMP propagation induced by two stimulatory G protein-coupled receptors in hearts
Proceedings of the National Academy of Sciences of the United States of America · 2012
75
cited
Protein Kinase Inhibitor Peptide as a Tool to Specifically Inhibit Protein Kinase A
Frontiers in Physiology · 2020
57
cited
Fatty Acid Oxidation Promotes Cardiomyocyte Proliferation Rate but Does Not Change Cardiomyocyte Number in Infant Mice
Front. Cell Dev. Biol. · 2019
53
cited
Abdominal Aortic Aneurysm Is a Specific Antigen‐Driven T Cell Disease
Annals of the New York Academy of Sciences · 2006
49
cited
Increasing Cardiac Contractility After Myocardial Infarction Exacerbates Cardiac Injury and Pump Dysfunction
Circulation Research · 2010
47
cited
Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.
American Journal of Physiology. Heart and Circulatory Physiology · 2010
42
cited
Reduced effects of BAY K 8644 on L-type Ca2+ current in failing human cardiac myocytes are related to abnormal adrenergic regulation.
American Journal of Physiology. Heart and Circulatory Physiology · 2008
42
cited
Cardiac G-Protein–Coupled Receptor Kinase 2 Ablation Induces a Novel Ca2+ Handling Phenotype Resistant to Adverse Alterations and Remodeling After Myocardial Infarction
Circulation · 2012
40
cited
Cardiomyocyte PKA Ablation Enhances Basal Contractility While Eliminates Cardiac β-Adrenergic Response Without Adverse Effects on the Heart.
Circulation Research · 2019
35
cited
Blunted cardiac beta-adrenergic response as an early indication of cardiac dysfunction in Duchenne muscular dystrophy.
Cardiovascular Research · 2014
33
cited
β-Adrenergic Stimulation Increases Cav3.1 Activity in Cardiac Myocytes through Protein Kinase A
PLoS ONE · 2012
32
cited
Persistent increases in Ca2+ influx through Cav1.2 shortens action potential and causes Ca2+ overload-induced afterdepolarizations and arrhythmias
Basic Research in Cardiology · 2015
30
cited
Increasing T‐type calcium channel activity by β‐adrenergic stimulation contributes to β‐adrenergic regulation of heart rates
Journal of Physiology · 2017
22
cited
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