ArticleEuropean journal of heart failure2012
Mechanical unloading reverses transverse tubule remodelling and normalizes local Ca(2+)-induced Ca(2+)release in a rodent model of heart failure.
Article in European journal of heart failure, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 88 citations in OpenAlex.
- Cardiac unloading models for myocardial reverse remodeling.Basic research in cardiology · 2026Review
- T-tubular remodeling occurs in a cardiomyocyte-autonomous manner following pathological mechanical stiffness exposure.Journal of molecular and cellular cardiology plus · 2026Article
- From function to structure: how myofibrillogenesis influences the transverse-axial tubular system development and its peculiarities.Frontiers in physiology · 2025Review
- Restoring Atrial T-Tubules Augments Systolic Ca Upon Recovery From Heart Failure.Circulation research · 2024Article
- Novel Targets for a Combination of Mechanical Unloading with Pharmacotherapy in Advanced Heart Failure.International journal of molecular sciences · 2022Review
- Ventricular reshaping with a beating heart implant improves pump function in experimental heart failure.The Journal of thoracic and cardiovascular surgery · 2022Article
- Cardiomyocyte Microtubules: Control of Mechanics, Transport, and Remodeling.Annual review of physiology · 2022Review
- Proposal for a trial of early left ventricular venting during venoarterial extracorporeal membrane oxygenation for cardiogenic shock.JTCVS open · 2021Article
- Role of t-tubule remodeling on mechanisms of abnormal calcium release during heart failure development in canine ventricle.American journal of physiology. Heart and circulatory physiology · 2021Article
- The mechanism of osmotically induced sealing of cardiac t tubules.American journal of physiology. Heart and circulatory physiology · 2020Article
- Nanoscale regulation of L-type calcium channels differentiates between ischemic and dilated cardiomyopathies.EBioMedicine · 2020Article
- Sodium-Glucose Cotransporter 2 Inhibitors Potentially Prevent Atrial Fibrillation by Ameliorating Ion Handling and Mitochondrial Dysfunction.Frontiers in physiology · 2020Review
- Severe T-System Remodeling in Pediatric Viral Myocarditis.Frontiers in cardiovascular medicine · 2020Article
- Influence of the tubular network on the characteristics of calcium transients in cardiac myocytes.PloS one · 2020Article
- Adverse transverse-tubule remodeling in a rat model of heart failure is attenuated with low-dose triiodothyronine treatment.Molecular medicine (Cambridge, Mass.) · 2019Article
- Biomimetic electromechanical stimulation to maintain adult myocardial slices in vitro.Nature communications · 2019Article
- Phosphodiesterase 5 inhibition improves contractile function and restores transverse tubule loss and catecholamine responsiveness in heart failure.Scientific reports · 2019Article
- Cardiomyocyte substructure reverts to an immature phenotype during heart failure.The Journal of physiology · 2019Article
- Partial Mechanical Unloading of the Heart Disrupts L-Type Calcium Channel and Beta-Adrenoceptor Signaling Microdomains.Frontiers in physiology · 2018Article
- Dyadic Plasticity in Cardiomyocytes.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
aimsCa(2+)-induced Ca(2+) release (CICR) is critical for contraction in cardiomyocytes. The transverse (t)-tubule system guarantees the proximity of the triggers for Ca(2+) release [L-type Ca(2+) channel, dihydropyridine receptors (DHPRs)] and the sarcoplasmic reticulum Ca(2+) 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 hypothesize that unloading of failing hearts normalizes t-tubule structure and improves CICR. METHODS AND
resultsHeart failure was induced in Lewis rats by left coronary artery ligation for 12 weeks; sham-operated animals were used as controls. Failing hearts were mechanically unloaded for 4 weeks by heterotopic abdominal heart transplantation (HF-UN). HF reduced the t-tubule density measured by di-8-ANEPPS staining in isolated left ventricular myocytes, and this was reversed by unloading. The deterioration in the regularity of the t-tubule system in HF was also reversed in HF-UN. Scanning ion conductance microscopy showed the reappearance of normal surface striations in HF-UN. Electron microscopy revealed recovery of normal t-tubule microarchitecture in HF-UN. L-type Ca(2+) current density, measured using whole-cell patch clamping, was reduced in HF but unaffected by unloading. The variance of the time-to-peak of the Ca(2+) transient, an index of CICR dyssynchrony, was increased in HF and normalized by unloading. The increased Ca(2+) spark frequency observed in HF was reduced in HF-UN. These results could be explained by the recoupling of orphaned RyRs in HF, as indicated by immunofluorescence.
conclusionsOur data show that mechanical unloading of the failing heart reverses the pathological remodelling of the t-tubule system and improves CICR.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.