ArticleCell reports2016
Microtubule-Dependent Mitochondria Alignment Regulates Calcium Release in Response to Nanomechanical Stimulus in Heart Myocytes.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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Who cites it
40 citing papers in PubMed.
- The roles of the microtubule cytoskeletal network in cardiac mechanobiology.Journal of cell science · 2026Review
- The mechanisms and therapeutic advances of interactions between breast cancer and cardiovascular diseases.Frontiers in pharmacology · 2026Review
- CCDC141 is a Connectin/Titin and Nesprin-1 binding protein that adapts cardiomyocytes to mechanical stress.Communications biology · 2025Article
- Mitochondria-derived vesicles: A promising and potential target for tumour therapy.Clinical and translational medicine · 2025Review
- Shape, membrane morphology, and morphodynamic response of metabolically active human mitochondria revealed by scanning ion conductance microscopy.Beilstein journal of nanotechnology · 2025Article
- Atrial myocyte senescence as a driver of atrial fibrillation: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Mitochondrial dysfunction as a central hub linking NaFrontiers in cardiovascular medicine · 2025Review
- Article
- RyR cooperativity and mobile buffers: functional clues to the resolution of the cardiac calcium wave problem?The Journal of physiology · 2024Article
- Restoring Atrial T-Tubules Augments Systolic Ca Upon Recovery From Heart Failure.Circulation research · 2024Article
- Diabetic Cardiomyopathy Uncovered: Transcriptomics, NLRP3, and Carvedilol Mechanisms.Journal of diabetes research · 2024Article
- Prevention of Atrial Fibrillation: Putting Proteostasis Derailment Back on Track.Journal of clinical medicine · 2023Review
- Delivery of mitochondria confers cardioprotection through mitochondria replenishment and metabolic compliance.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Advances in Ion Channel, Non-Desmosomal Variants and Autophagic Mechanisms Implicated in Arrhythmogenic Cardiomyopathy.Current issues in molecular biology · 2023Review
- Alterations in Cytoskeleton and Mitochondria in the Development and Reversal of Steatosis in Human Hepatocytes.Cellular and molecular gastroenterology and hepatology · 2023Article
- Intrinsic cell rheology drives junction maturation.Nature communications · 2022Article
- TECRL deficiency results in aberrant mitochondrial function in cardiomyocytes.Communications biology · 2022Article
- Compartmentalized cAMP signaling in cardiac ventricular myocytes.Cellular signalling · 2022Review
- Mechanisms of cAMP compartmentation in cardiac myocytes: experimental and computational approaches to understanding.The Journal of physiology · 2021Review
- Mitochondrial dynamics, positioning and function mediated by cytoskeletal interactions.Cellular and molecular life sciences : CMLS · 2021Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Arrhythmogenesis during heart failure is a major clinical problem. Regional electrical gradients produce arrhythmias, and cellular ionic transmembrane gradients are its originators. We investigated whether the nanoscale mechanosensitive properties of cardiomyocytes from failing hearts have a bearing upon the initiation of abnormal electrical activity. Hydrojets through a nanopipette indent specific locations on the sarcolemma and initiate intracellular calcium release in both healthy and heart failure cardiomyocytes, as well as in human failing cardiomyocytes. In healthy cells, calcium is locally confined, whereas in failing cardiomyocytes, calcium propagates. Heart failure progressively stiffens the membrane and displaces sub-sarcolemmal mitochondria. Colchicine in healthy cells mimics the failing condition by stiffening the cells, disrupting microtubules, shifting mitochondria, and causing calcium release. Uncoupling the mitochondrial proton gradient abolished calcium initiation in both failing and colchicine-treated cells. We propose the disruption of microtubule-dependent mitochondrial mechanosensor microdomains as a mechanism for abnormal calcium release in failing heart.
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