Protective effect and mechanism of estrogen receptor β on myocardial infarction in mice

Zhang, Junbiao; Guo, Chang-Jun

doi:10.3892/etm.2017.4628

Cited by 7 publications

(3 citation statements)

References 30 publications

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“…In addition, ERβ mediates cardioprotection in I/R on OVX mice through the PI3K/Akt pathway and anti-apoptotic signaling (decreased caspase-3 and -8 activities and increased Bcl-2) [ 64 ] and diminishes post-MI fibrosis [ 26 , 61 ]. ERβ could also influence arrhythmogenesis after MI, as infarcted females with ERβ deficiency show prolongation of ventricular repolarization and reduction in automaticity [ 65 ].…”

Section: Er Modulation and Mi: Preclinical Studiesmentioning

confidence: 99%

Estrogen Receptors: Therapeutic Perspectives for the Treatment of Cardiac Dysfunction after Myocardial Infarction

Montagnoli

Rocha

et al. 2021

IJMS

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Estrogen receptors (ER) mediate functions beyond their endocrine roles, as modulation of cardiovascular, renal, and immune systems through anti-inflammatory and anti-apoptotic effects, preventing necrosis of cardiomyocytes and endothelial cells, and attenuating cardiac hypertrophy. Estradiol (E2) prevents cardiac dysfunction, increases nitric oxide synthesis, and reduces the proliferation of vascular cells, yielding protective effects, regardless of gender. Such actions are mediated by ER (ER-alpha (ERα), ER-beta (ERβ), or G protein-coupled ER (GPER)) through genomic or non-genomic pathways, which regulate cardiovascular function and prevent tissue remodeling. Despite the extensive knowledge on the cardioprotective effects of estrogen, clinical studies conducted on myocardial infarction (MI) and cardiovascular diseases still include favorable and unfavorable profiles. The purpose of this review is to provide up-to-date information regarding molecular, preclinical, and clinical aspects of cardiovascular E2 effects and ER modulation as a potential therapeutic target for the treatment of MI-induced cardiac dysfunction.

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Section: Er Modulation and Mi: Preclinical Studiesmentioning

confidence: 99%

Estrogen Receptors: Therapeutic Perspectives for the Treatment of Cardiac Dysfunction after Myocardial Infarction

Montagnoli

Rocha

et al. 2021

IJMS

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“…A recent study shows that rat cardiac fibroblast ER-α activation by E2 leads to inhibition of collagen I and III production in females, while E2 binding to ER-β promotes collagen production in males (51). However, another study shows that increased levels of ER-β after MI protect from inflammation and fibrosis formation in female mice (52). These studies do not have to be conflictive seeing that ER-α and -β dimerization inhibits collagen deposition, and an increased ER-β concentration could amplify this (51).…”

Section: (Perivascular) Fibrosis Formationmentioning

confidence: 99%

Estrogen Contributions to Microvascular Dysfunction Evolving to Heart Failure With Preserved Ejection Fraction

et al. 2019

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Heart failure with preserved ejection fraction (HFpEF) is a syndrome involving microvascular dysfunction. No treatment is available yet and as the HFpEF patient group is expanding due to the aging population, more knowledge on dysfunction of the cardiac microvasculature is required. Endothelial dysfunction, impaired angiogenesis, (perivascular) fibrosis and the pruning of capillaries (rarefaction) may all contribute to microvascular dysfunction in the heart and other organs, e.g., the kidneys. The HFpEF patient group consists mainly of post-menopausal women and female sex itself is a risk factor for this syndrome. This may point toward a role of estrogen depletion after menopause in the development of HFpEF. Estrogens favor the ratio of vasodilating over vasoconstricting factors, which results in an overall lower blood pressure in women than in men. Furthermore, estrogens improve angiogenic capacity and attenuate (perivascular) fibrosis formation. Therefore, we hypothesize that the drop of estrogen levels after menopause contributes to myocardial microvascular dysfunction and renders post-menopausal women more vulnerable for heart diseases that involve the microvasculature. This review provides a detailed summary of molecular targets of estrogen, which might guide future research and treatment options.

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“…In recent years, in vivo and in vitro experiments have proven that the compound has positive anticancer, anti-inflammatory, antioxidative, neuroprotective, myocardial-protective, liver-protective, and kidney-protective effects ( 73 , 74 ). In addition, it has been reported that salidroside can inhibit the release of lactate dehydrogenase (LDH), creatine-kinase (CK) and aspartate aminotransferase (AST) from human cardiomyocytes by increasing the expression of HIF-1α, increasing the content of superoxide dismutase (SOD), increasing the activity of human cardiomyocytes, and reducing the death and apoptosis of cells ( 75 ). Overall, it was speculated that the main composition of RW may play a significant role in the treatment of AP through hub targets in these top-ranking signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Investigating the multitarget pharmacological mechanism of Rhodiola wallichiana var. cholaensis acting on angina pectoris using combined network pharmacology and molecular docking

Zhang,

Zhuang,

et al. 2024

J Thorac Dis

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Background Rhodiola wallichiana var. cholaensis (RW) is one of the traditional Chinese medicinal materials, which is used to treat angina pectoris (AP). However, the possible underlying mechanisms remains unclear. The aim of this study was to explore RW in the treatment of AP and to identify the potential mechanism of the core compounds. Methods In this study, systematic and comprehensive network pharmacology and molecular docking were used for the first time to explore the potential pharmacological mechanisms of RW on AP. First, the relative compounds were obtained by mining the literature, and potential targets of these compounds using target prediction were collected. We then built the AP target database using the DigSee and GeneCards databases. Based on the data, overlapping targets and hub genes were identified with Maximal Clique Centrality (MCC) algorithm in Cytoscape, cytoHubba. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses and protein-protein interaction (PPI) analysis were performed to screen the hub targets by topology. Molecular docking was utilized to investigate the receptor-ligand interactions on Autodock Vina and visualized in PyMOL. Results A total of 218 known RW therapeutic targets were selected. Systematic analysis identified nine hub targets ( VEGFA , GAPDH , TP53 , AKT1 , CASP3 , STAT3 , TNF , MAPK1 and JUN ) mainly involved in the complex treatment effects associated with the protection of the vascular endothelium, as well as the regulation of glucose metabolism, cellular processes, inflammatory responses, and cellular signal transduction. Molecular docking indicated that the core compounds had good affinity with the core targets. Conclusions The results of this study preliminarily identify the potential targets and signaling pathways of RW in AP therapy and lay a promising foundation for further experimental studies and clinical trials.

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Protective effect and mechanism of estrogen receptor β on myocardial infarction in mice

Cited by 7 publications

References 30 publications

Estrogen Receptors: Therapeutic Perspectives for the Treatment of Cardiac Dysfunction after Myocardial Infarction

Estrogen Receptors: Therapeutic Perspectives for the Treatment of Cardiac Dysfunction after Myocardial Infarction

Estrogen Contributions to Microvascular Dysfunction Evolving to Heart Failure With Preserved Ejection Fraction

Investigating the multitarget pharmacological mechanism of Rhodiola wallichiana var. cholaensis acting on angina pectoris using combined network pharmacology and molecular docking

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