ArticleCardiovascular research2024
Endothelial oestrogen-myocardial cyclic guanosine monophosphate axis critically determines angiogenesis and cardiac performance during pressure overload.
Article in Cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Novel Quality Metrics for Assessing the Reproducibility and Translational Relevance of Mouse Transverse Aortic Constriction Experiments: A Systematic Review.Journal of the American Heart Association · 2026Pooled it
- Efficacy of the new P100 extracorporeal shock wave therapy device in the treatment of type IIIB chronic prostatitis/chronic pelvic pain syndrome: a sham treatment controlled, prospective clinical trial.Prostate cancer and prostatic diseases · 2026Trial
- Panax quinquefolium saponin decreases atherosclerosis in ovariectomized ApoEChinese medicine · 2026Article
- Inhibition of adenosine kinase alleviates hypertrophic cardiomyopathy by ameliorating coronary microvascular dysfunction.ESC heart failure · 2026Article
- Targeting Integrin β3 in Endothelial Cells Attenuates Cardiac Fibrosis Through the Calcium-Calmodulin-Dependent Protein Kinase IIα- cAMP-Responsive Element Binding Protein 1 Signaling Axis in Pressure Overload-Induced Heart Failure.Journal of the American Heart Association · 2026Article
- Cardiomyocyte GC1 Mediates Estrogenic Angiogenesis in Right Heart Remodeling.Circulation research · 2025Article
- Pathogenic glycosyltransferase genes and potential therapeutic drugs in pressure overload-induced heart failure.ESC heart failure · 2025Article
- NIR light-propelled Janus Polydopamine@Mesoporous silica gene delivery nanomotor for the enhanced gene treatment of critical limb ischemia.Materials today. Bio · 2025Article
- Advances in humanoid organoid-based research on inter-organ communications during cardiac organogenesis and cardiovascular diseases.Journal of translational medicine · 2025Review
- KMV-mediated cardiomyocyte-to-endothelial cell signaling drives capillary rarefaction to promote heart failure following pressure overload.Theranostics · 2025Article
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12 authors.
Funding
Abstract
aimsOestrogen exerts beneficial cardiovascular effects by binding to specific receptors on various cells to activate nuclear and non-nuclear actions. Oestrogen receptor α (ERα) non-nuclear signalling confers protection against heart failure remodelling, involving myocardial cyclic guanosine monophosphate (cGMP)-cGMP-dependent protein kinase G (PKG) activation; however, its tissue-specific role remains elusive. Herein, we examine the cell type-specific role of ERα non-nuclear signalling in oestrogen-conferred protection against heart failure. METHODS AND
resultsWe first assessed the tissue-specific impacts of ERα on the cardiac benefits derived from oestrogen, utilizing endothelial ERα deletion (ERαf/f/Tie2Cre+) and myocyte ERα deletion (ERαf/f/αMHCCre+) female mice. Female mice were ovariectomized and the effect of estradiol (E2) was assessed in hearts exposed to 3 weeks of pressure overload [transverse aortic constriction (TAC)]. E2 failed to improve cardiac function in ERαf/f/Tie2Cre+ TAC hearts but provided benefits in ERαf/f/αMHCCre+ TAC hearts, indicating that endothelial ERα is essential. We next assessed the role of non-nuclear signalling in endothelial cells (ECs), employing animals with endothelial-specific inactivation of ERα non-nuclear signalling (ERαKI/KI/Tie2Cre+). Female ovariectomized mice were supplemented with E2 and subjected to 3-week TAC. ERαKI/KI/Tie2Cre+TAC hearts revealed exacerbated cardiac dysfunction and reduced myocardial PKG activity as compared to littermate TAC hearts, which were associated with attenuated myocardial induction of vascular endothelial growth factor (VEGF) and angiogenesis as assessed by CD31-stained capillary density. This phenotype of ERαKI/KI/Tie2Cre+was rescued by myocardial PKG activation from chronic treatment with a soluble guanylate cyclase (sGC) stimulator. We performed co-culture experiments to determine endothelial-cardiomyocyte interactions. VEGF induction by E2 in cardiac myocytes required a co-existence of intact endothelial ERα signalling in a nitric oxide synthase-dependent manner. On the other hand, VEGF was induced in myocytes directly with an sGC stimulator in the absence of ECs.
conclusionAn endothelial oestrogen-myocardial cGMP axis stimulates angiogenic response and improves cardiac performance during pressure overload.
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