2012
DOI: 10.1093/eurjhf/hfs038
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Abstract: Aims Ca2+‐induced Ca2+ release (CICR) is critical for contraction in cardiomyocytes. The transverse (t)‐tubule system guarantees the proximity of the triggers for Ca2+ release [L‐type Ca2+ channel, dihydropyridine receptors (DHPRs)] and the sarcoplasmic reticulum Ca2+ release channels [ryanodine receptors (RyRs)]. Transverse tubule disruption occurs early in heart failure (HF). Clinical studies of left ventricular assist devices in HF indicate that mechanical unloading induces reverse remodelling. We hypothesi… Show more

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Cited by 74 publications
(69 citation statements)
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References 51 publications
(100 reference statements)
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“…These studies motivated us to apply this marker in the investigations on the myocardial tissue from VAD patients. Unlike the disruption of the t-tubule system that was observed by Ibrahim et al (5) in rat hearts that were fully unloaded (and denervated) after heterotopic transplantation, in the case of the partial unloading induced by VADs, we did not observe any t-tubule system changes that would indicate atrophic In an effort to investigate whether signaling pathways associated with atrophic remodeling were activated, we performed an extensive molecular analysis.…”
Section: Myocardial Atrophymentioning
confidence: 66%
“…These studies motivated us to apply this marker in the investigations on the myocardial tissue from VAD patients. Unlike the disruption of the t-tubule system that was observed by Ibrahim et al (5) in rat hearts that were fully unloaded (and denervated) after heterotopic transplantation, in the case of the partial unloading induced by VADs, we did not observe any t-tubule system changes that would indicate atrophic In an effort to investigate whether signaling pathways associated with atrophic remodeling were activated, we performed an extensive molecular analysis.…”
Section: Myocardial Atrophymentioning
confidence: 66%
“…23 Thus, we report a new finding with fundamental mechanistic importance: unlike pressure-overload LV hypertrophy, TT disruption is not an inherent feature of left ventricular hypertrophy induced by volume overload hemodynamic stress, but occurs during the transition to heart failure in Wave mice with aortic regurgitation. Future studies, using techniques which overcome the limited resolution of light microscopy 25 , may reveal disturbances within individual TT that occur in volume-overload left ventricular hypertrophy and heart failure. EGFR-tk signaling is trophic for LV myocardium, as overexpression produces cardiomyocyte enlargement and increased LV mass, 26 whereas EGFR-tk deficiency results in LV wall thinning and decreased contractility.…”
Section: Discussionmentioning
confidence: 99%
“…Conversely, too much stress as experienced in heart failure appears to be a driver for pathological remodelling; for example, high-stress regions near infarct sites typically have a low abundance of t-tubules (Frisk et al 2016). Direct evidence for this mechanism was demonstrated by mechanical unloading of the ischaemic failing heart in the rat by heterotopic abdominal heart transplantation; this procedure reversed t-tubule remodelling and normalised local Ca 2+ release (Ibrahim et al 2012). The same procedure used for prolonged mechanical unloading of normal hearts led to loss of t-tubule structure and impaired Ca 2+ signalling (Ibrahim et al 2010), indicating that there is a 'Goldilocks zone' of mechanical load.…”
Section: Mechanisms Of T-tubule Remodellingmentioning
confidence: 99%