Response by Benitah et al to Letter Regarding Article, “Orai1 Channel Inhibition Preserves Left Ventricular Systolic Function and Normal Ca 2+ Handling After Pressure Overload”-Reference-Cited by-同舟云学术

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Response by Benitah et al to Letter Regarding Article, “Orai1 Channel Inhibition Preserves Left Ventricular Systolic Function and Normal Ca 2+ Handling After Pressure Overload”

Published:2020-06-02 Issue:22 Volume:141 Page:
ISSN:0009-7322
Container-title:Circulation
language:en
Short-container-title:Circulation

Author:

Benitah Jean-Pierre¹,Beech David J.²,Sabourin Jessica¹

Affiliation:

1. Inserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (J.P.B., J.S.).

2. Leeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (D.J.B.).

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

Reference5 articles.

1. Orai1 Channel Inhibition Preserves Left Ventricular Systolic Function and Normal Ca 2+ Handling After Pressure Overload

2. Unveiling some FDA-approved drugs as inhibitors of the store-operated Ca2+ entry pathway

3. CRAC channels as targets for drug discovery and development

4. Cardiac Remodeling and Disease: SOCE and TRPC Signaling in Cardiac Pathology

5. Inhibition of Hypertrophy, Per Se, May Not Be a Good Therapeutic Strategy in Ventricular Pressure Overload: Other Approaches Could Be More Beneficial

Cited by 1 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. Targeting Orai1-Mediated Store-Operated Ca2+ Entry in Heart Failure;Frontiers in Cell and Developmental Biology;2020-10-08

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