ArticleCirculation2020
Orai1 Channel Inhibition Preserves Left Ventricular Systolic Function and Normal Ca
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Article in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41citing papers in PubMed
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41 citing papers in PubMed, 57 citations in OpenAlex.
- Research progress on the role and mechanism of STIM and Orai protein-mediated store-operated calcium entry in cardiovascular diseases.Channels (Austin, Tex.) · 2026Review
- Local calcium dynamics and signalling in cardiomyocytes.Nature reviews. Cardiology · 2026Review
- ZBED6 deficiency drives pathological cardiac hypertrophy through MEOX1-ERK1/2-dependent autophagy dysfunction.PLoS genetics · 2026Article
- Calcium Signaling in Cardiac Fibroblasts: Roles in Fibrosis and Therapeutic Implications.Cardiovascular drugs and therapy · 2026Review
- Calcium Signaling Dysregulation in Diabetic Cardiomyopathy: Roles of STIM and Orai Channels.Handbook of experimental pharmacology · 2026Review
- A rare ORAI1 missense variant associates with risk of vascular diseases in White British adults.PloS one · 2026Article
- Combination of Orai1 inhibitor CM5480 with specific therapy mitigates pulmonary hypertension and its cardiac dysfunction.JCI insight · 2025Article
- Early cardioprotective effects of SGLT2i on hypertensive cardiac remodeling via STIM1/Orai1-dependent calcium signaling: beyond blood pressure control.Journal of bioenergetics and biomembranes · 2025Article
- Orai channel pharmacological manipulation reduces metabolic flexibility in cardiac fibroblasts.American journal of physiology. Cell physiology · 2025Article
- Inhibition of adenylyl cyclase 8 prevents the upregulation of Orai1 channel, which improves cardiac function after myocardial infarction.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- ORAI1 inhibition as an efficient preclinical therapy for tubular aggregate myopathy and Stormorken syndrome.JCI insight · 2024Article
- Side-by-side comparison of published small molecule inhibitors against thapsigargin-induced store-operated Ca2+ entry in HEK293 cells.PloS one · 2024Article
- Store-Operated Calcium Entry Increases Nuclear Calcium in Adult Rat Atrial and Ventricular Cardiomyocytes.Cells · 2023Article
- Searching for Effective Treatments in HFpEF: Implications for Modeling the Disease in Rodents.Pharmaceuticals (Basel, Switzerland) · 2023Review
- The Mechanism of the Anti-Cardiac Hypertrophy Effect of Glycyrrhizic Acid Is Related to Reducing STIM1-Dependent Store-Operated Calcium Entry.Bulletin of experimental biology and medicine · 2023Article
- ORAI Calcium Channels: Regulation, Function, Pharmacology, and Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2023Review
- The SOCE Machinery: An Unbalanced Knowledge between Left and Right Ventricular Pathophysiology.Cells · 2022Review
- Proteomic mapping and optogenetic manipulation of membrane contact sites.The Biochemical journal · 2022Article
- Sex-specific differences in cardiac function, inflammation and injury during early polymicrobial sepsis.Intensive care medicine experimental · 2022Article
- CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype.EMBO molecular medicine · 2022Article
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Authors and funding
26 authors at 2 institutions in 2 countries.
Fiona BartoliInserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (F.B., P.M., K.B., P.G., S.G., F.L., A.-M.G., J.P.B., J. Sabourin).
Marc A BaileyLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Baptiste RodeLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Philippe MateoInserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (F.B., P.M., K.B., P.G., S.G., F.L., A.-M.G., J.P.B., J. Sabourin).
Fabrice AntignyInserm, UMR-S 999, Université Paris-Saclay, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France (F.A., C.R.M.).
Kaveen BedouetInserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (F.B., P.M., K.B., P.G., S.G., F.L., A.-M.G., J.P.B., J. Sabourin).
Pascale GerbaudInserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (F.B., P.M., K.B., P.G., S.G., F.L., A.-M.G., J.P.B., J. Sabourin).
Rajendra GosainSchool of Chemistry, University of Leeds, United Kingdom (R.G., J.P., K.N., R.F.).
Jeffrey PlanteSchool of Chemistry, University of Leeds, United Kingdom (R.G., J.P., K.N., R.F.).
Katherine NormanSchool of Chemistry, University of Leeds, United Kingdom (R.G., J.P., K.N., R.F.).
Susana GomezInserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (F.B., P.M., K.B., P.G., S.G., F.L., A.-M.G., J.P.B., J. Sabourin).
Florence LefebvreInserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (F.B., P.M., K.B., P.G., S.G., F.L., A.-M.G., J.P.B., J. Sabourin).
Catherine Rucker-MartinInserm, UMR-S 999, Université Paris-Saclay, Centre Chirurgical Marie Lannelongue, Le Plessis-Robinson, France (F.A., C.R.M.).
Justin F X AinscoughLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Mark T KearneyLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Alexander-Francisco BrunsLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Jian ShiLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Hollie L ApplebyLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Richard S YoungLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Heba M ShawerLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Marjolaine DebantLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Ana-Maria GomezInserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (F.B., P.M., K.B., P.G., S.G., F.L., A.-M.G., J.P.B., J. Sabourin).
David J BeechLeeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, United Kingdom (M.A.B., B.R., J.F.X.A., M.T.K., A.-F.B., J. Shi, H.L.A., R.S.Y., H.M.S., M.D., D.J.B.).
Richard FosterSchool of Chemistry, University of Leeds, United Kingdom (R.G., J.P., K.N., R.F.).
Jean-Pierre BenitahInserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (F.B., P.M., K.B., P.G., S.G., F.L., A.-M.G., J.P.B., J. Sabourin).
Jessica SabourinInserm, UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France (F.B., P.M., K.B., P.G., S.G., F.L., A.-M.G., J.P.B., J. Sabourin).
University of Leeds · GBInserm · FR
Funding
British Heart Foundation CH/13/1/30086British Heart Foundation FS/12/54/29671British Heart Foundation FS/13/23/30122British Heart Foundation FS/17/2/32559British Heart Foundation FS/18/12/33270British Heart Foundation RG/15/7/31521British Heart Foundation RG/17/11/33042Cancer Research UKMedical Research Council G1002076Medical Research Council MC_PC_14109Medical Research Council MR/L019051/1
Abstract
backgroundOrai1 is a critical ion channel subunit, best recognized as a mediator of store-operated Ca
methodsTo test the role of these Orai1 channels in the cardiac pathophysiology, a transgenic mouse was generated with cardiomyocyte-specific expression of an ion pore-disruptive Orai1
resultsAdult mice subjected to transverse aortic constriction (TAC) developed cardiac hypertrophy and reduced ventricular function associated with increased Orai1 expression and Orai1-dependent SOCE (assessed by Mn
conclusionsThe findings suggest a key role of cardiac Orai1 channels and the potential for Orai1 channel inhibitors as inotropic therapies for maintaining contractility reserve after hypertrophic stress.
Indexed as
Calcium SignalingVentricular Function, LeftAnimalsCalciumCardiomegalyFocal Adhesion Kinase 2MiceMice, TransgenicMyocytes, CardiacORAI1 ProteinSarcoplasmic Reticulum Calcium-Transporting ATPasesCalciumFocal Adhesion Kinase 2ORAI1 ProteinOrai1 protein, mousePtk2b protein, mouseSarcoplasmic Reticulum Calcium-Transporting ATPasescalciumcardiomyocyteshypertrophyORAI1 proteinventricular function
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