Xiaoying Zhang

发表

GDF11 does not rescue aging-related pathological hypertrophy.

S. Houser, M. Franti, S. Mohsin, 2015, Circulation research.

Cardiotoxic and Cardioprotective Features of Chronic &bgr;-Adrenergic Signaling

F. Wang, Hui Gao, E. Gao, 2013, Circulation research.

Activation or inhibition of PPARα-mediated fatty acid β-oxidation does not active cardiomyocyte proliferation in normal or infarcted adult mice

Ying Tian, E. Gao, Rajika Roy, 2019, bioRxiv.

Fatty Acid Oxidation Promotes Cardiomyocyte Proliferation Rate but Does Not Change Cardiomyocyte Number in Infant Mice

D. Liccardo, Tongtong Cao, Ying Tian, 2019, Front. Cell Dev. Biol..

Cardiovascular Pharmacology: Open Access β-adrenergic System and Cardiac Physiology and Pathophysiology

Xiongwen Chen, Xiaoying Zhang, Yingxin Li, 2013 .

ÃÂ²-adrenergic System and Cardiac Physiology and Pathophysiology

Xiongwen Chen, Xiaoying Zhang, Yingxin Li, 2012 .

Reduced effects of BAY K 8644 on L-type Ca2+ current in failing human cardiac myocytes are related to abnormal adrenergic regulation.

David M. Harris, S. Houser, K. Margulies, 2008, American journal of physiology. Heart and circulatory physiology.

Adolescent Feline Heart Contains a Population of Small, Proliferative Ventricular Myocytes With Immature Physiological Properties

David M. Harris, S. Houser, C. Bearzi, 2007, Circulation research.

Cardiac GRK2 Ablation Induces a Novel Ca Handling Phenotype Resistant to Adverse Alterations and Remodeling After Myocardial Infarction

S. Houser, G. Dorn, W. Koch, 2012 .

Heart Failure Cardiac G-Protein–Coupled Receptor Kinase 2 Ablation Induces a Novel Ca Handling Phenotype Resistant to Adverse Alterations and Remodeling After Myocardial Infarction

S. Houser, G. Dorn, W. Koch, 2012 .

Ca Influx–Induced Sarcoplasmic Reticulum Ca 2 (cid:1) Overload Causes Mitochondrial-Dependent Apoptosis in Ventricular Myocytes Cellular Biology

David M. Harris, S. Houser, Xiongwen Chen, 2005 .

Increasing Cardiac Contractility After Myocardial Infarction Exacerbates Cardiac Injury and Pump Dysfunction

David M. Harris, S. Houser, W. Koch, 2009, Circulation research.

Increasing T‐type calcium channel activity by β‐adrenergic stimulation contributes to β‐adrenergic regulation of heart rates

S. Houser, J. Molkentin, M. Xie, 2017, The Journal of physiology.

Cardiomyocyte PKA Ablation Enhances Basal Contractility While Eliminates Cardiac β-Adrenergic Response Without Adverse Effects on the Heart.

S. Houser, Daohai Yu, Ying Tian, 2019, Circulation research.

Acetylation of SERCA2a, Another Target for Heart Failure Treatment?

S. Houser, J. Soboloff, Xiongwen Chen, 2019, Circulation research.

Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.

S. Houser, H. Nakayama, J. Molkentin, 2010, American journal of physiology. Heart and circulatory physiology.

PKI-GFP Prevents Cardiac Dysfunction and Myocyte Death Induced by ISO

Naresh, F. Wang, Hui Gao, 2013 .

β-Adrenergic Stimulation Increases Cav3.1 Activity in Cardiac Myocytes through Protein Kinase A

Y. Li, Mingxin Tang, Xiongwen Chen, 2012, PloS one.

Ca2+ Influx–Induced Sarcoplasmic Reticulum Ca2+ Overload Causes Mitochondrial-Dependent Apoptosis in Ventricular Myocytes

David M. Harris, S. Houser, Xiongwen Chen, 2005, Circulation research.

Protein Kinase Inhibitor Peptide as a Tool to Specifically Inhibit Protein Kinase A

Xiongwen Chen, Xiaoying Zhang, Chong Liu, 2020, Frontiers in Physiology.

Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure.

T. Hewett, S. Houser, H. Nakayama, 2007, The Journal of clinical investigation.

Phosphodiesterases coordinate cAMP propagation induced by two stimulatory G protein-coupled receptors in hearts

X. Zhang, D. Parikh, Y. Li, 2012, Proceedings of the National Academy of Sciences.

Hepatic PKA inhibition accelerates the lipid accumulation in liver

M. Mi, C. Zeng, Xiongwen Chen, 2019, Nutrition & Metabolism.

Blunted cardiac beta-adrenergic response as an early indication of cardiac dysfunction in Duchenne muscular dystrophy.

Daohai Yu, S. Ge, Xiongwen Chen, 2014, Cardiovascular research.

Cardiac G-Protein–Coupled Receptor Kinase 2 Ablation Induces a Novel Ca2+ Handling Phenotype Resistant to Adverse Alterations and Remodeling After Myocardial Infarction

S. Houser, G. Dorn, W. Koch, 2012, Circulation.

MICU1-dependent mitochondrial calcium uptake regulates lung alveolar type 2 cell plasticity and lung regeneration

Mir Ali, Ying Tian, D. Tomar, 2022, JCI insight.

Cross talk between serine/threonine and tyrosine kinases regulates ADP-induced thromboxane generation in platelets

X. Zhang, S. Kunapuli, Y. Senis, 2015, Thrombosis and Haemostasis.

A low voltage activated Ca2+ current found in a subset of human ventricular myocytes

David M. Harris, S. Houser, K. Margulies, 2020, Channels.

Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.

David M. Harris, S. Houser, W. Koch, 2011, Journal of molecular and cellular cardiology.

Reduced Myocardial Reserve in Young X‐Linked Muscular Dystrophy Mice Diagnosed by Two‐Dimensional Strain Analysis Combined with Stress Echocardiography

Longjian Liu, S. Ge, Xiongwen Chen, 2017, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.

Abdominal Aortic Aneurysm Is a Specific Antigen‐Driven T Cell Disease

John V. White, D. Monos, J. Gaughan, 2006, Annals of the New York Academy of Sciences.

Systemic Hypoxemia Induces Cardiomyocyte Hypertrophy and Right Ventricular Specific Induction of Proliferation

S. Houser, Ying Tian, S. Mohsin, 2023, Circulation research.

Persistent increases in Ca2+ influx through Cav1.2 shortens action potential and causes Ca2+ overload-induced afterdepolarizations and arrhythmias

David M. Harris, W. Koch, H. Nakayama, 2015, Basic Research in Cardiology.

Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress

R. Weiss, Long-Sheng Song, C. Franzini-armstrong, 2014, Proceedings of the National Academy of Sciences.

Fatty Acid Oxidation Promotes Cardiomyocyte Proliferation Rate but Does Not Change Cardiomyocyte Number in Infant Mice

D. Liccardo, Tongtong Cao, Ying Tian, 2019, Front. Cell Dev. Biol..

Increasing Cardiac Contractility After Myocardial Infarction Exacerbates Cardiac Injury and Pump Dysfunction

David M. Harris, S. Houser, W. Koch, 2010, Circulation research.

Reduced effects of BAY K 8644 on L-type Ca2+ current in failing human cardiac myocytes are related to abnormal adrenergic regulation.

David M. Harris, S. Houser, K. Margulies, 2008, American journal of physiology. Heart and circulatory physiology.

Cav3.1/α1G T-Type Ca2+ Channels are Involved in the Heart Rate Regulation

J. Molkentin, F. Wang, Mingxin Tang, 2011 .

Cardiotoxic and Cardioprotective Features of Chronic β -Adrenergic Signaling

Naresh, F. Wang, Hui Gao, 2013 .

Cardiotoxic and Cardioprotective Features of Chronic β -Adrenergic Signaling

S. Kunapuli, Mingxin Tang, Xiongwen Chen, 2013 .

Protein Kinase A Is a Master Regulator of Physiological and Pathological Cardiac Hypertrophy

S. Houser, Mingxin Tang, Xiongwen Chen, 2024, Circulation research.