ArticleCardiovascular research2017
Increased collagen within the transverse tubules in human heart failure.
Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 71 citations in OpenAlex.
- Endotrophin is a risk marker of complications in CANagliflozin cardioVascular Assessment Study (CANVAS): a randomized controlled trial.Cardiovascular diabetology · 2022Trial
- T-tubular remodeling occurs in a cardiomyocyte-autonomous manner following pathological mechanical stiffness exposure.Journal of molecular and cellular cardiology plus · 2026Article
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- Calcium handling remodeling in dilated cardiomyopathy: From molecular mechanisms to targeted therapies.Channels (Austin, Tex.) · 2025Review
- Left ventricular myocardial molecular profile of human diabetic ischaemic cardiomyopathy.EMBO molecular medicine · 2025Article
- Proteome Alterations in Cardiac Fibroblasts: Insights from Experimental Myocardial Infarction and Clinical Ischaemic Cardiomyopathy.International journal of molecular sciences · 2025Article
- Review
- From function to structure: how myofibrillogenesis influences the transverse-axial tubular system development and its peculiarities.Frontiers in physiology · 2025Review
- Proteomic and metabolomic analyses of the human adult myocardium reveal ventricle-specific regulation in end-stage cardiomyopathies.Communications biology · 2024Article
- The Efficacy of Risk Factor Modification Compared to NADJACC. Basic to translational science · 2024Article
- Matriglycan maintains t-tubule structural integrity in cardiac muscle.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Ptpn23 Controls Cardiac T-Tubule Patterning by Promoting the Assembly of Dystrophin-Glycoprotein Complex.Circulation · 2024Article
- Pirfenidone increases transverse tubule length in the infarcted rat myocardium.Interface focus · 2023Article
- Changes of calcium cycling in HFrEF and HFpEF.Mechanobiology in medicine · 2023Review
- Ryanodine Receptor Staining Identifies Viable Cardiomyocytes in Human and Rabbit Cardiac Tissue Slices.International journal of molecular sciences · 2023Article
- The heterocellular heart: identities, interactions, and implications for cardiology.Basic research in cardiology · 2023Review
- Specific and label-free endogenous signature of dystrophic muscle by Synchrotron deep ultraviolet radiation.Scientific reports · 2023Article
- Serial block face scanning electron microscopy reveals region-dependent remodelling of transverse tubules post-myocardial infarction.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
- Article
- Fibrosis and impaired CaBiophysical reviews · 2022Article
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Authors and funding
13 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsIn heart failure transverse-tubule (t-tubule) remodelling disrupts calcium release, and contraction. T-tubules in human failing hearts exhibit increased labelling by wheat germ agglutinin (WGA), a lectin that binds to the dystrophin-associated glycoprotein complex. We hypothesized changes in this complex may explain the increased WGA labelling and contribute to t-tubule remodelling in the failing human heart. In this study we sought to identify the molecules responsible for this increased WGA labelling. METHODS AND
resultsConfocal and super-resolution fluorescence microscopy and proteomic analyses were used to quantify left ventricle samples from healthy donors and patients with idiopathic dilated cardiomyopathy (IDCM). Confocal microscopy demonstrated both WGA and dystrophin were located at t-tubules. Super-resolution microscopy revealed that WGA labelling of t-tubules is largely located within the lumen while dystrophin was restricted to near the sarcolemma. Western blots probed with WGA reveal a 5.7-fold increase in a 140 kDa band in IDCM. Mass spectrometry identified this band as type VI collagen (Col-VI) comprised of α1(VI), α2(VI), and α3(VI) chains. Pertinently, mutations in Col-VI cause muscular dystrophy. Western blotting identified a 2.4-fold increased expression and 3.2-fold increased WGA binding of Col-VI in IDCM. Confocal images showed that Col-VI is located in the t-tubules and that their diameter increased in the IDCM samples. Super-resolution imaging revealed Col-VI was restricted to the t-tubule lumen where increases were associated with displacement in the sarcolemma as identified from dystrophin labelling. Samples were also labelled for type I, III, and IV collagen. Both confocal and super-resolution imaging identified that these collagens were also present within t-tubule lumen.
conclusionIncreased expression and labelling of collagen in IDCM samples indicates fibrosis may contribute to t-tubule remodelling in human heart failure.
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