ArticleCirculation research2017
Role of STIM1 (Stromal Interaction Molecule 1) in Hypertrophy-Related Contractile Dysfunction.
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Article in Circulation research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32citing papers in PubMed
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Who cites it
32 citing papers in PubMed.
- Research progress on the role and mechanism of STIM and Orai protein-mediated store-operated calcium entry in cardiovascular diseases.Channels (Austin, Tex.) · 2026Review
- STIM1-dependent treg dysfunction promotes cardiometabolic HFpEF: insights from patients and animal studies.Cardiovascular diabetology · 2026Article
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Calcium Signaling Dysregulation in Diabetic Cardiomyopathy: Roles of STIM and Orai Channels.Handbook of experimental pharmacology · 2026Review
- Store-Operated Calcium Entry Increases Nuclear Calcium in Adult Rat Atrial and Ventricular Cardiomyocytes.Cells · 2023Article
- Role of STIM1 in the Regulation of Cardiac Energy Substrate Preference.International journal of molecular sciences · 2023Review
- STIM1 ablation impairs exercise-induced physiological cardiac hypertrophy and dysregulates autophagy in mouse hearts.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- The SOCE Machinery: An Unbalanced Knowledge between Left and Right Ventricular Pathophysiology.Cells · 2022Review
- Cardiac Hypertrophy: From Pathophysiological Mechanisms to Heart Failure Development.Reviews in cardiovascular medicine · 2022Review
- Left ventricular hypertrophy and sudden cardiac death.Heart failure reviews · 2022Review
- Analysis ofAmerican journal of physiology. Heart and circulatory physiology · 2022Article
- STIM and Orai Mediated Regulation of Calcium Signaling in Age-Related Diseases.Frontiers in aging · 2022Review
- Obesity cardiomyopathy: evidence, mechanisms, and therapeutic implications.Physiological reviews · 2021Review
- Amelioration of circadian disruption and calcium-handling protein defects by choline alleviates cardiac remodeling in abdominal aorta coarctation rats.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Pyridostigmine improves cardiac function and rhythmicity through RyR2 stabilization and inhibition of STIM1-mediated calcium entry in heart failure.Journal of cellular and molecular medicine · 2021Article
- Cardiac-Specific Deletion of Orai3 Leads to Severe Dilated Cardiomyopathy and Heart Failure in Mice.Journal of the American Heart Association · 2021Article
- SOCE in the cardiomyocyte: the secret is in the chambers.Pflugers Archiv : European journal of physiology · 2021Review
- Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021Review
- Review
- Is the sigma-1 receptor a potential pharmacological target for cardiac pathologies? A systematic review.International journal of cardiology. Heart & vasculature · 2020Review
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Authors and funding
11 authors.
Constantine D TroupesFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Markus WallnerFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Giulia BorghettiFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Chen ZhangFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Sadia MohsinFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Dirk von LewinskiFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Remus M BerrettaFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Hajime KuboFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Xiongwen ChenFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Jonathan SoboloffFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.).
Steven HouserFrom the Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (C.D.T., M.W., G.B., C.Z., S.M., R.M.B., H.K., X.C., S.H.); Department of Cardiology, Medical University of Graz, Austria (D.v.L.); and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University School of Medicine, Philadelphia, PA (J.S.). srhouser@temple.edu.
Funding
Calcium and Cardiac Regeneration after Myocardial InfarctionR01HL033921 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI HOUSER, STEVEN R · 1985 to 2017
$5.6MCONTRACTILITY OF FAILING AND RECOVERING HUMAN MYOCYTESR01HL061495 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI HOUSER, STEVEN R · 1998 to 2006
$3.1MEGR-mediated STIM1-PMCA expression and function in T cell subsetsR01GM117907 · NIGMS · TEMPLE UNIV OF THE COMMONWEALTH · PI SOBOLOFF, JONATHAN A · 2016 to 2019
$1.6MNHLBI NIH HHS R01 HL033921NHLBI NIH HHS R01 HL061495NIGMS NIH HHS R01 GM117907
Abstract
rationalePathological increases in cardiac afterload result in myocyte hypertrophy with changes in myocyte electrical and mechanical phenotype. Remodeling of contractile and signaling Ca
objectiveTo define the contributions of STIM1-mediated Ca METHODS AND
resultsCardiac hypertrophy was induced by slow progressive pressure overload in adult cats. Hypertrophied myocytes had increased STIM1 expression and activity, which correlated with altered Ca
conclusionsSTIM1 can associate with Orai in cardiac myocytes to produce a Ca
Indexed as
Action PotentialsAnimalsCardiomegalyCatsCells, CulturedMaleMyocardial ContractionNeoplasm ProteinsStromal Interaction Molecule 1Neoplasm ProteinsSTIM1 protein, humanStromal Interaction Molecule 1calciummyocytes, cardiacstromal interaction molecule 1
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.