Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium.
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Acute Myocardial Response to Stretch: What We (don't) KnowThe autocrine/paracrine loop after myocardial stretch: mineralocorticoid receptor activationSilencing of NHE-1 blunts the slow force response to myocardial stretchSilencing of cardiac mitochondrial NHE1 prevents mitochondrial permeability transition pore opening.Endothelin signalling regulates volume-sensitive Cl- current via NADPH oxidase and mitochondrial reactive oxygen speciesA highly sensitive chemiluminescence assay for superoxide detection and chronic granulomatous disease diagnosis.Mechanosignaling in the vasculature: emerging concepts in sensing, transduction and physiological responsesThrombospondins in the transition from myocardial infarction to heart failure.Epidermal Growth Factor Receptor Silencing Blunts the Slow Force Response to Myocardial Stretch.Hyperactive adverse mechanical stress responses in dystrophic heart are coupled to transient receptor potential canonical 6 and blocked by cGMP-protein kinase G modulation.Role of autocrine/paracrine mechanisms in response to myocardial strain.Physiological regulation of cardiac contractility by endogenous reactive oxygen species.Regulation of the cardiac sodium/bicarbonate cotransporter by angiotensin II: potential Contribution to structural, ionic and electrophysiological myocardial remodelling.Cell adhesion markedly increases lucigenin-enhanced chemiluminescence of the phagocyte NADPH oxidase.Mitochondrial NHE1: a newly identified target to prevent heart disease.Mineralocorticoid receptor activation is crucial in the signalling pathway leading to the Anrep effect.The role of nitric oxide and reactive oxygen species in the positive inotropic response to mechanical stretch in the mammalian myocardium.The Anrep effect requires transactivation of the epidermal growth factor receptor.In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy.Endogenous endothelin 1 mediates angiotensin II-induced hypertrophy in electrically paced cardiac myocytes through EGFR transactivation, reactive oxygen species and NHE-1.Chronic NHE-1 blockade induces an antiapoptotic effect in the hypertrophied heart.Na+/H+ exchanger-1 inhibitors decrease myocardial superoxide production via direct mitochondrial action.TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca(2+) concentration in mouse cardiomyocytes.Inhibition of carbonic anhydrase prevents the Na(+)/H(+) exchanger 1-dependent slow force response to rat myocardial stretch.RETRACTED: Compensatory role of the NBCn1 sodium/bicarbonate cotransporter on Ca2+-induced mitochondrial swelling in hypertrophic hearts.
P2860
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P2860
Mitochondrial reactive oxygen species activate the slow force response to stretch in feline myocardium.
description
2007 nî lūn-bûn
@nan
2007年の論文
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2007年学术文章
@wuu
2007年学术文章
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2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
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2007年學術文章
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2007年學術文章
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name
Mitochondrial reactive oxygen ...... stretch in feline myocardium.
@en
Mitochondrial reactive oxygen ...... stretch in feline myocardium.
@nl
type
label
Mitochondrial reactive oxygen ...... stretch in feline myocardium.
@en
Mitochondrial reactive oxygen ...... stretch in feline myocardium.
@nl
prefLabel
Mitochondrial reactive oxygen ...... stretch in feline myocardium.
@en
Mitochondrial reactive oxygen ...... stretch in feline myocardium.
@nl
P2093
P2860
P1476
Mitochondrial reactive oxygen ...... stretch in feline myocardium.
@en
P2093
Alejandra M Yeves
Carolina D Garciarena
Claudia I Caldiz
Gladys Chiappe de Cingolani
Leonardo P Novaretto
Néstor G Pérez
Raúl A Dulce
P2860
P304
P356
10.1113/JPHYSIOL.2007.141689
P407
P577
2007-09-06T00:00:00Z