ArticleThe Journal of endocrinology2017
Glucocorticoid receptor alters isovolumetric contraction and restrains cardiac fibrosis.
Article in The Journal of endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Enhancing anti-fibrotic therapy: nanomedicine approaches to overcome current limitations.Materials today. Bio · 2026Review
- Inter-Organ Communication Networks in Systemic Physiology: Glucocorticoid Receptor α as a Central Integrator of Homeostasis.International journal of molecular sciences · 2026Review
- Exploring Anti-Inflammatory Treatment as Upstream Therapy in the Management of Atrial Fibrillation.Journal of clinical medicine · 2025Review
- New insights into the roles of glucocorticoid signaling dysregulation in pathological cardiac hypertrophy.Heart failure reviews · 2022Review
- Network modeling predicts personalized gene expression and drug responses in valve myofibroblasts cultured with patient sera.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Corticosteroid Receptors in Cardiac Health and Disease.Advances in experimental medicine and biology · 2022Article
- Physical Activity Engagement Worsens Health Outcomes and Limits Exercise Capacity in Growth-restricted Mice.Medicine and science in sports and exercise · 2021Article
- Alcohol consumption, depression, overweight and cortisol levels as determining factors for NR3C1 gene methylation.Scientific reports · 2021Article
- Long-term administration of prednisolone: Effects on the myocardial tissue of healthy beagle dogs.The Journal of veterinary medical science · 2021Article
- Glucocorticoids preserve the t-tubular system in ventricular cardiomyocytes by upregulation of autophagic flux.Basic research in cardiology · 2019Article
- Deletion of the Cardiomyocyte Glucocorticoid Receptor Leads to Sexually Dimorphic Changes in Cardiac Gene Expression and Progression to Heart Failure.Journal of the American Heart Association · 2019Article
- Antenatal dexamethasone treatment transiently alters diastolic function in the mouse fetal heart.The Journal of endocrinology · 2019Article
- Cardiomyocyte glucocorticoid and mineralocorticoid receptors directly and antagonistically regulate heart disease in mice.Science signaling · 2019Article
- Glucocorticoids, antenatal corticosteroid therapy and fetal heart maturation.Journal of molecular endocrinology · 2018Review
- Glucocorticoid Signaling in Health and Disease: Insights From Tissue-Specific GR Knockout Mice.Endocrinology · 2018Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Corticosteroids directly affect the heart and vasculature and are implicated in the pathogenesis of heart failure. Attention is focussed upon the role of the mineralocorticoid receptor (MR) in mediating pro-fibrotic and other adverse effects of corticosteroids upon the heart. In contrast, the role of the glucocorticoid receptor (GR) in the heart and vasculature is less well understood. We addressed this in mice with cardiomyocyte and vascular smooth muscle deletion of GR (SMGRKO mice). Survival of SMGRKO mice to weaning was reduced compared with that of littermate controls. Doppler measurements of blood flow across the mitral valve showed an elongated isovolumetric contraction time in surviving adult SMGRKO mice, indicating impairment of the initial left ventricular contractile phase. Although heart weight was elevated in both genders, only male SMGRKO mice showed evidence of pathological cardiomyocyte hypertrophy, associated with increased myosin heavy chain-β expression. Left ventricular fibrosis, evident in both genders, was associated with elevated levels of mRNA encoding MR as well as proteins involved in cardiac remodelling and fibrosis. However, MR antagonism with spironolactone from birth only modestly attenuated the increase in pro-fibrotic gene expression in SMGRKO mice, suggesting that elevated MR signalling is not the primary driver of cardiac fibrosis in SMGRKO mice, and cardiac fibrosis can be dissociated from MR activation. Thus, GR contributes to systolic function and restrains normal cardiac growth, the latter through gender-specific mechanisms. Our findings suggest the GR:MR balance is critical in corticosteroid signalling in specific cardiac cell types.
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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.