17beta-estradiol reduces cardiomyocyte apoptosis in vivo and in vitro via activation of phospho-inositide-3 kinase/Akt signaling. - Wikidata - awgldk - TriplyDB

17beta-estradiol reduces cardiomyocyte apoptosis in vivo and in vitro via activation of phospho-inositide-3 kinase/Akt signaling.

17beta-estradiol reduces cardiomyocyte apoptosis in vivo and in vitro via activation of phospho-inositide-3 kinase/Akt signaling.

http://www.wikidata.org/entity/Q45042583

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Cardiovascular imaging: what have we learned from animal models?Effects of biological sex on the pathophysiology of the heart Estrogen, aging and the cardiovascular system Estrogen deficiency decreases ischemic tolerance in the aged rat heart: Roles of PKCdelta, PKCepsilon, Akt, and GSK3beta Mechanistic Pathways of Sex Differences in Cardiovascular Disease.A mechanistic study of the effect of doxorubicin/adriamycin on the estrogen response in a breast cancer model Membrane initiated estrogen signaling in breast cancer.Female sex and estrogen receptor-beta attenuate cardiac remodeling and apoptosis in pressure overload.Neisseria gonorrhoeae survival during primary human cervical epithelial cell infection requires nitric oxide and is augmented by progesterone Influence of sex hormones and phytoestrogens on heart disease in men and women Cardiomyocyte-specific Estrogen Receptor Alpha Increases Angiogenesis, Lymphangiogenesis and Reduces Fibrosis in the Female Mouse Heart Post-Myocardial Infarction.The cholesterol metabolite 25-hydroxycholesterol activates estrogen receptor α-mediated signaling in cancer cells and in cardiomyocytes Female adult mouse cardiomyocytes are protected against oxidative stress.Potential phytoestrogen alternatives exert cardio-protective mechanisms via estrogen receptors Sex-related resistance to myocardial ischemia-reperfusion injury is associated with high constitutive ARC expression Hormonal regulation of cardiac KCNE2 gene expression.Direct and indirect protection of right ventricular function by estrogen in an experimental model of pulmonary arterial hypertension.Estradiol increases angiotensin II type 1 receptor in hearts of ovariectomized rats.Oestrogen prevents cardiomyocyte apoptosis by suppressing p38α-mediated activation of p53 and by down-regulating p53 inhibition on p38β.An association between gene expression and better survival in female mice following myocardial infarction.Testosterone-down-regulated Akt pathway during cardiac ischemia/reperfusion: a mechanism involving BAD, Bcl-2 and FOXO3a.Evidence that the G protein-coupled membrane receptor GPR30 contributes to the cardiovascular actions of estrogen.17 Beta-estradiol differentially affects left ventricular and cardiomyocyte hypertrophy following myocardial infarction and pressure overload Role of biological sex in normal cardiac function and in its disease outcome - a review Estrogen-induced apoptosis of breast epithelial cells is blocked by NO/cGMP and mediated by extranuclear estrogen receptors.Estrogen receptor activation and cardioprotection in ischemia reperfusion injury.Estrogen prevents cardiomyocyte apoptosis through inhibition of reactive oxygen species and differential regulation of p38 kinase isoforms.Oestrogen-mediated cardioprotection following ischaemia and reperfusion is mimicked by an oestrogen receptor (ER)alpha agonist and unaffected by an ER beta antagonist.Estrogen signaling in the cardiovascular system.Nuclear targeting of Akt antagonizes aspects of cardiomyocyte hypertrophy.Endocytosis of HERG is clathrin-independent and involves arf6.Estrogen-induced SDF-1 production is mediated by estrogen receptor-α in female hearts after acute ischemia and reperfusion.Mitochondrial maintenance failure in aging and role of sexual dimorphism.Decreased metalloprotease 9 induction, cardiac fibrosis, and higher autophagy after pressure overload in mice lacking the transcriptional regulator p8.Estrogen attenuates left ventricular and cardiomyocyte hypertrophy by an estrogen receptor-dependent pathway that increases calcineurin degradation.Loss of receptor activity-modifying protein 3 exacerbates cardiac hypertrophy and transition to heart failure in a sex-dependent manner.Pro-survival effects of 17β-estradiol on osteocytes are mediated by nitric oxide/cGMP via differential actions of cGMP-dependent protein kinases I and II G Protein-Coupled Estrogen Receptor 1 Mediates Acute Estrogen-Induced Cardioprotection via MEK/ERK/GSK-3β Pathway after Ischemia/Reperfusion.Membrane estrogen receptor alpha is an important modulator of bone marrow C-Kit+ cells mediated cardiac repair after myocardial infarction.Qiliqiangxin improves cardiac function and attenuates cardiac remodeling in rats with experimental myocardial infarction.

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17beta-estradiol reduces cardiomyocyte apoptosis in vivo and in vitro via activation of phospho-inositide-3 kinase/Akt signaling.

http://www.wikidata.org/entity/Q45042583

description

2004 nî lūn-bûn

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2004年の論文

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年学术文章

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2004年學術文章

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2004年學術文章

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name

17beta-estradiol reduces cardi ...... sitide-3 kinase/Akt signaling.

@en

17beta-estradiol reduces cardi ...... sitide-3 kinase/Akt signaling.

@nl

type

label

17beta-estradiol reduces cardi ...... sitide-3 kinase/Akt signaling.

@en

17beta-estradiol reduces cardi ...... sitide-3 kinase/Akt signaling.

@nl

prefLabel

17beta-estradiol reduces cardi ...... sitide-3 kinase/Akt signaling.

@en

17beta-estradiol reduces cardi ...... sitide-3 kinase/Akt signaling.

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17beta-estradiol reduces cardi ...... sitide-3 kinase/Akt signaling.

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Ashour Michael

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Christian Grohe

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Flore Celestin

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Isaac Pourati

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Jason Baur

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Mark J Aronovitz

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Michael E Mendelsohn

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Richard D Patten

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Richard H Karas

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scholarly article

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