ArticleEuropean journal of pharmacology2011
Dexamethasone induces transcriptional activation of Bcl-xL gene and inhibits cardiac injury by myocardial ischemia.
Article in European journal of pharmacology, 2011. 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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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- Cardiomyocyte derived extracellular mitochondria in activation of macrophages during oxidative stress.Cardiovascular research · 2026Article
- Cedrol mitigates hepatic lipid accumulation and adipocyte hypertrophy induced by corticosteroids through the inhibition of glucocorticoid receptor activity.Scientific reports · 2025Article
- Timing of RAS blocker administration and long-term cardiovascular outcomes in STEMI patients.Herz · 2025Observational
- Plasmapheresis as a Potential Generalizable Therapy for Myocardial Infarction.Rejuvenation research · 2025Review
- Adrenal Insufficiency Associated Cardiomyopathy, From Molecule to Clinic: A Comprehensive Review.Health science reports · 2025Article
- Macrophage heterogeneity in myocardial infarction: Evolution and implications for diverse therapeutic approaches.iScience · 2024Review
- Efficacy of preoperative single-dose dexamethasone in preventing postoperative pulmonary complications following minimally invasive esophagectomy: a retrospective propensity score-matched study.Perioperative medicine (London, England) · 2024Article
- Long-term Dexamethasone Treatment Increases Cardiac Galectin-3 Levels.Cardiovascular drugs and therapy · 2023Article
- The Development of Novel Drug Treatments for Stroke Patients: A Review.International journal of molecular sciences · 2022Review
- Chemotherapy-Free Targeted Anti-BCR-ABL+ Acute Lymphoblastic Leukemia Therapy May Benefit the Heart.Cancers · 2022Article
- Case report: Changes in the levels of stress hormones during Takotsubo syndrome.Frontiers in cardiovascular medicine · 2022Article
- Dexamethasone Alleviates Myocardial Injury in a Rat Model of Acute Myocardial Infarction Supported by Venoarterial Extracorporeal Membrane Oxygenation.Frontiers in public health · 2022Article
- Histone methyltransferase KMT2D contributes to the protection of myocardial ischemic injury.Frontiers in cell and developmental biology · 2022Article
- Benefits of combined exercise training on arterial stiffness and blood pressure in spontaneously hypertensive rats treated or not with dexamethasone.Frontiers in physiology · 2022Article
- Corticosteroid Receptors in Cardiac Health and Disease.Advances in experimental medicine and biology · 2022Article
- The effect of docetaxel on survival, fertilization rate and apoptosis-related genes mRNA expression in mouse metaphase II oocytes following vitrification.Iranian journal of veterinary research · 2021Article
- Review
- Glucocorticoids preserve the t-tubular system in ventricular cardiomyocytes by upregulation of autophagic flux.Basic research in cardiology · 2019Article
- Review
- Anti-inflammatory therapies in myocardial infarction: failures, hopes and challenges.British journal of pharmacology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Psychological or physical stress causes an elevation of glucocorticoids in the circulating system. Glucocorticoids regulate a variety of physiological functions, from energy metabolism and biochemical homeostasis to immune response. Synthetic steroids are among the most prescribed drugs for immune suppression and chemotherapy. While glucocorticoids are best known for inducing apoptosis in a number of cell types, we have found that corticosteroids at stress relevant levels protect cardiomyocytes from apoptosis. Current study addresses whether glucocorticoids inhibit cardiac injury in vivo. Adult male C57BL6 mice were administered with dexamethasone (20mg/kg, i.p.) or vehicle control 20 h prior to left anterior descending coronary artery occlusion surgery. Myocardial infarction was measured by triphenyl tetrazoliumchloride staining in tissue slices and by levels of cardiac Troponin (cTn I) in the blood. Treatment of dexamethasone markedly reduced infarct size (19.6 ± 4.3%, vs. 29.2 ± 4.9%, p<0.01) and cTn I level in the blood (3.83 ± 0.66 ng/ml vs. 5.62 ± 0.37 ng/ml, p<0.01). In studying the mechanism of such protection, we found that dexamethasone induces the expression of Bcl-xL gene in the myocardium. With cardiomyocytes in culture, glucocorticoids increased transcription of Bcl-xL gene as evidenced by Bcl-xL mRNA increase and promoter activation. The glucocorticoid receptor antagonist mifepristone prevented dexamethasone from inducing cardiac protection or Bcl-xL expression. Our data suggest that activation of glucocorticoid receptor can prevent cardiac injury through transcriptional activation of Bcl-xL gene.
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Registered trials
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