ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
The sarcoplasmic reticulum luminal thiol oxidase ERO1 regulates cardiomyocyte excitation-coupled calcium release and response to hemodynamic load.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Endoplasmic reticulum oxidoreductin 1α as a potential therapeutic target in diseases: from oxidative protein folding to pathophysiological mechanisms.Frontiers in pharmacology · 2025Review
- ERO1A levels are a prognostic indicator in EGFR mutated non small cell lung cancer.NPJ precision oncology · 2024Article
- Extracellular vesicles from human cardiac stromal cells up-regulate cardiomyocyte protective responses to hypoxia.Stem cell research & therapy · 2024Article
- Endoplasmic reticular stress as an emerging therapeutic target for chronic pain: a narrative review.British journal of anaesthesia · 2024Review
- SEPN1-related myopathy depends on the oxidoreductase ERO1A and is druggable with the chemical chaperone TUDCA.Cell reports. Medicine · 2024Article
- Biological mechanisms and clinical significance of endoplasmic reticulum oxidoreductase 1 alpha (ERO1α) in human cancer.Journal of experimental & clinical cancer research : CR · 2024Review
- Editorial: The role of calcium and calcium binding proteins in cell physiology and disease.Frontiers in physiology · 2023Article
- Loss-of-rescue of Ryr1Scientific reports · 2022Article
- Ero1α-Dependent ERp44 Dissociation From RyR2 Contributes to Cardiac Arrhythmia.Circulation research · 2022Article
- The role of mitochondria-associated membranes mediated ROS on NLRP3 inflammasome in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Review
- Endoplasmic reticulum as a target in cardiovascular diseases: Is there a role for flavonoids?Frontiers in pharmacology · 2022Review
- ER stress and calcium-dependent arrhythmias.Frontiers in physiology · 2022Review
- ERO1-PDI Redox Signaling in Health and Disease.Antioxidants & redox signaling · 2021Review
- The ER stress response mediator ERO1 triggers cancer metastasis by favoring the angiogenic switch in hypoxic conditions.Oncogene · 2021Article
- Structure and Function of Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs) and Their Role in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2021Review
- Role of the ERO1-PDI interaction in oxidative protein folding and disease.Pharmacology & therapeutics · 2020Review
- Mesencephalic astrocyte-derived neurotrophic factor is an ER-resident chaperone that protects against reductive stress in the heart.The Journal of biological chemistry · 2020Article
- Analysis of the characteristics and expression profiles of coding and noncoding RNAs of human dental pulp stem cells in hypoxic conditions.Stem cell research & therapy · 2019Article
- Homocysteine causes vascular endothelial dysfunction by disrupting endoplasmic reticulum redox homeostasis.Redox biology · 2019Article
- A maladaptive ER stress response triggers dysfunction in highly active muscles of mice with SELENON loss.Redox biology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Two related ER oxidation 1 (ERO1) proteins, ERO1α and ERO1β, dynamically regulate the redox environment in the mammalian endoplasmic reticulum (ER). Redox changes in cysteine residues on intralumenal loops of calcium release and reuptake channels have been implicated in altered calcium release and reuptake. These findings led us to hypothesize that altered ERO1 activity may affect cardiac functions that are dependent on intracellular calcium flux. We established mouse lines with loss of function insertion mutations in Ero1l and Ero1lb encoding ERO1α and ERO1β. The peak amplitude of calcium transients in homozygous Ero1α mutant adult cardiomyocytes was reduced to 42.0 ± 2.2% (n=10, P ≤ 0.01) of values recorded in wild-type cardiomyocytes. Decreased ERO1 activity blunted cardiomyocyte inotropic response to adrenergic stimulation and sensitized mice to adrenergic blockade. Whereas all 12 wild-type mice survived challenge with 4 mg/kg esmolol, 6 of 8 compound Ero1l and Ero1lb mutant mice succumbed to this level of β adrenergic blockade (P ≤ 0.01). In addition, mice lacking ERO1α were partially protected against progressive heart failure in a transaortic constriction model [at 10 wk postprocedure, fractional shortening was 0.31 ± 0.02 in the mutant (n=20) vs. 0.23 ± 0.03 in the wild type (n=18); P ≤ 0.01]. These findings establish a role for ERO1 in calcium homeostasis and suggest that modifying the lumenal redox environment may affect the progression of heart failure.
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Registered trials
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.