Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy-Reference-Cited by-同舟云学术

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

Published:2011-03 Issue:3 Volume:50 Page:460-470
ISSN:0022-2828
Container-title:Journal of Molecular and Cellular Cardiology
language:en
Short-container-title:Journal of Molecular and Cellular Cardiology

Author:

Chen Xiongwen,Nakayama Hiroyuki,Zhang Xiaoying,Ai Xiaojie,Harris David M.,Tang Mingxin,Zhang Hongyu,Szeto Christopher,Stockbower Kathryn,Berretta Remus M.,Eckhart Andrea D.,Koch Walter J.,Molkentin Jeffery D.,Houser Steven R.

Publisher

Elsevier BV

Subject

Cardiology and Cardiovascular Medicine,Molecular Biology

Reference34 articles.

1. Regulation of cardiac hypertrophy by intracellular signalling pathways;Heineke;Nat Rev Mol Cell Biol,2006

2. Beta-adrenergic function in heart muscle disease and heart failure;Bristow;J Mol Cell Cardiol,1985

3. Adrenergic pathways and left ventricular remodeling;Dorn;J Card Fail,2002

4. Calmodulin kinase II inhibition protects against structural heart disease;Zhang;Nat Med,2005

5. Physical and functional interaction between calcineurin and the cardiac L-type Ca2+ channel;Tandan;Circ Res,2009

Cited by 98 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. Cell size induced bias of current density in hypertrophic cardiomyocytes;Channels;2024-06-05

2. Protein Kinase A Is a Master Regulator of Physiological and Pathological Cardiac Hypertrophy;Circulation Research;2024-02-16

3. Dysregulated Rbfox2 produces aberrant splicing of CaV1.2 calcium channel in diabetes-induced cardiac hypertrophy;Cardiovascular Diabetology;2023-07-06

4. Calcium Handling Remodeling Underlies Impaired Sympathetic Stress Response in Ventricular Myocardium from Cacna1c Haploinsufficient Rats;International Journal of Molecular Sciences;2023-06-06

5. Combining three independent pathological stressors induces a heart failure with preserved ejection fraction phenotype;American Journal of Physiology-Heart and Circulatory Physiology;2023-04-01