Increased exchange current but normal Ca2+ transport via Na+-Ca2+ exchange during cardiac hypertrophy after myocardial infarction.
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FKBP12.6 overexpression decreases Ca2+ spark amplitude but enhances [Ca2+]i transient in rat cardiac myocytes.Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress.Chronic heart rate reduction with ivabradine improves systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term increase in FKBP12/12.6 expression.Heart failure -- a challenge to our current concepts of excitation-contraction coupling.The long QT interval is not only inherited but is also linked to cardiac hypertrophy.Reconciling depressed Ca2+ sparks occurrence with enhanced RyR2 activity in failing mice cardiomyocytes.ACE inhibition prevents diastolic Ca2+ overload and loss of myofilament Ca2+ sensitivity after myocardial infarction.Subcellular remodeling as a viable target for the treatment of congestive heart failure.Conditional mineralocorticoid receptor expression in the heart leads to life-threatening arrhythmias.New modes of exchanger regulation: physiological implications.Myofilament calcium de-sensitization and contractile uncoupling prevent pause-triggered ventricular tachycardia in mouse hearts with chronic myocardial infarctionColony-stimulating factor-1 transfection of myoblasts improves the repair of failing myocardium following autologous myoblast transplantation.Myocardial infarction causes increased expression but decreased activity of the myocardial Na+-Ca2+ exchanger in the rabbit.Increased Ca(2+) leak and spatiotemporal coherence of Ca(2+) release in cardiomyocytes during beta-adrenergic stimulation.Sprint training improves contractility in postinfarction rat myocytes: role of Na+/Ca2+ exchange.Effects of Na+/Ca2+ exchange induced by SR Ca2+ release on action potentials and afterdepolarizations in guinea pig ventricular myocytes.Modification of sarcolemmal Na+-K+-ATPase and Na+/Ca2+ exchanger expression in heart failure by blockade of renin-angiotensin system.Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats.
P2860
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P2860
Increased exchange current but normal Ca2+ transport via Na+-Ca2+ exchange during cardiac hypertrophy after myocardial infarction.
description
2002 nî lūn-bûn
@nan
2002 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2002 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2002年の論文
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2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
name
Increased exchange current but ...... y after myocardial infarction.
@ast
Increased exchange current but ...... y after myocardial infarction.
@en
type
label
Increased exchange current but ...... y after myocardial infarction.
@ast
Increased exchange current but ...... y after myocardial infarction.
@en
prefLabel
Increased exchange current but ...... y after myocardial infarction.
@ast
Increased exchange current but ...... y after myocardial infarction.
@en
P2093
P50
P1433
P1476
Increased exchange current but ...... hy after myocardial infarction
@en
P2093
Ana Maria Gómez
Guy Vassort
Hartmut Porzig
P304
P356
10.1161/01.RES.0000031384.55006.DB
P577
2002-08-01T00:00:00Z