Hongyu Zhang

发表

T-type Ca2+ channels regulate the exit of cardiac myocytes from the cell cycle after birth

S. Houser, Hui Gao, Catherine A Makarewich, 2013, Journal of molecular and cellular cardiology.

Generation of effective vaccines against liver cancer by using photodynamic therapy

Ying-xin Li, Hongyu Zhang, Wen-jiang Ma, 2009, Lasers in Medical Science.

Hyperphosphorylation of the Cardiac Ryanodine Receptor at Serine 2808 Is Not Involved in Cardiac Dysfunction After Myocardial Infarction

S. Houser, W. Koch, E. Gao, 2012, Circulation research.

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

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

Integrative Hyperphosphorylation of the Cardiac Ryanodine Receptor at Serine 2808 Is Not Involved in Cardiac Dysfunction After Myocardial Infarction

S. Houser, Y. Li, W. Koch, 2012 .

A Caveolae-Targeted L-Type Ca2+ Channel Antagonist Inhibits Hypertrophic Signaling Without Reducing Cardiac Contractility

S. Houser, J. Molkentin, Hui Gao, 2012, 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.

Caspase-1 mediates hyperlipidemia-weakened progenitor cell vessel repair.

S. Houser, M. Madesh, D. Tilley, 2016, Frontiers in bioscience.

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

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

{beta}1-Adrenergic receptor activation induces mouse cardiac myocyte death through both L-type calcium channel-dependent and -independent pathways.

S. Houser, Hui Gao, Xiongwen Chen, 2010, American journal of physiology. Heart and circulatory physiology.

Effect of Laser and LED on Enzymatic Production of Ceramide

Xuebing Xu, P. Buchhave, Ying-xin Li, 2011, Photochemistry and photobiology.

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.

Metronomic photodynamic therapy with 5-aminolevulinic acid induces apoptosis and autophagy in human SW837 colorectal cancer cells.

Weichao Liu, Yingxin Li, H. Yin, 2019, Journal of photochemistry and photobiology. B, Biology.

TIPE2 acts as a negative regulator linking NOD2 and inflammatory responses in myocardial ischemia/reperfusion injury

Ziying Wang, P. Ren, Ye Chen, 2015, Journal of Molecular Medicine.

Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling.

S. Houser, J. Molkentin, Hui Gao, 2012, Journal of molecular and cellular cardiology.

Ca2+ Influx Through T- and L-Type Ca2+ Channels Have Different Effects on Myocyte Contractility and Induce Unique Cardiac Phenotypes

S. Houser, H. Nakayama, J. Molkentin, 2008, Circulation research.

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.

STIM1 elevation in the heart results in aberrant Ca²⁺ handling and cardiomyopathy.

S. Houser, J. Molkentin, J. V. van Berlo, 2015, Journal of molecular and cellular cardiology.

Transient Receptor Potential Channels Contribute to Pathological Structural and Functional Remodeling After Myocardial Infarction

S. Houser, M. Madesh, J. Molkentin, 2014, Circulation research.

Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.

Donald M Bers, Steven R Houser, Franz Hofmann, 2012, The Journal of clinical investigation.

(cid:1) 1 -Adrenergic receptor activation induces mouse cardiac myocyte death through both L-type calcium channel-dependent and -independent pathways

S. Houser, Hui Gao, Xiongwen Chen, 2010 .

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.

Caveolae-localized L-type Ca2+ channels do not contribute to function or hypertrophic signalling in the mouse heart

S. Houser, J. Molkentin, Robert N. Correll, 2017, Cardiovascular research.

UltraRapid Communication A Caveolae-Targeted L-Type Ca 2 Channel Antagonist Inhibits Hypertrophic Signaling Without Reducing Cardiac Contractility

S. Houser, J. Molkentin, Hui Gao, 2017 .

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

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

Hyperphosphorylation of the Cardiac Ryanodine Receptor at Serine 2808 Is Not Involved in Cardiac Dysfunction After Myocardial Infarction

S. Houser, W. Koch, E. Gao, 2012, Circulation research.

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

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

Integrative Hyperphosphorylation of the Cardiac Ryanodine Receptor at Serine 2808 Is Not Involved in Cardiac Dysfunction After Myocardial Infarction

S. Houser, Y. Li, W. Koch, 2012 .

Integrative Hyperphosphorylation of the Cardiac Ryanodine Receptor at Serine 2808 Is Not Involved in Cardiac Dysfunction After Myocardial Infarction

S. Houser, Xiongwen Chen, H. Kubo, 2012 .