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

• Published in: Circulation (New York, N.Y.) Vol. 141; no. 3; pp. 199 - 216
• Main Authors: Bartoli, Fiona, Bailey, Marc A., Rode, Baptiste, Mateo, Philippe, Antigny, Fabrice, Bedouet, Kaveen, Gerbaud, Pascale, Gosain, Rajendra, Plante, Jeffrey, Norman, Katherine, Gomez, Susana, Lefebvre, Florence, Rucker-Martin, Catherine, Ainscough, Justin F.X., Kearney, Mark T., Bruns, Alexander-Francisco, Shi, Jian, Appleby, Hollie L., Young, Richard S., Shawer, Heba M., Debant, Marjolaine, Gomez, Ana-Maria, Beech, David J., Foster, Richard, Benitah, Jean-Pierre, Sabourin, Jessica
• Format: Journal Article
• Language: English
• Published: United States American Heart Association 21.01.2020
• Subjects: Animals; Calcium - metabolism; Calcium Signaling; Cardiomegaly - genetics; Cardiomegaly - metabolism; Cardiomegaly - pathology; Focal Adhesion Kinase 2 - genetics; Focal Adhesion Kinase 2 - metabolism; Life Sciences; Mice; Mice, Transgenic; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - pathology; ORAI1 Protein - antagonists & inhibitors; ORAI1 Protein - genetics; ORAI1 Protein - metabolism; Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics; Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism; Ventricular Function, Left; cardiomyocytes; calcium; ORAI1 protein; hypertrophy; ventricular function

Orai1 is a critical ion channel subunit, best recognized as a mediator of store-operated Ca entry (SOCE) in nonexcitable cells. SOCE has recently emerged as a key contributor of cardiac hypertrophy and heart failure but the relevance of Orai1 is still unclear. To test the role of these Orai1 channel...