ArticleThe Journal of physiology2020
Quantitative tests reveal that microtubules tune the healthy heart but underlie arrhythmias in pathology.
Article in The Journal of physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Role of NADPH oxidase 2-derived reactive oxygen species in cardiac electrophysiological disorders.Channels (Austin, Tex.) · 2026Review
- Vasohibin 1 acts as a key regulator of arrhythmogenesis in pressure-overload-induced cardiac hypertrophy.Acta pharmacologica Sinica · 2026Article
- Tubulin Post-Translational Modifications in Cardiovascular Diseases: Emerging Mechanisms and Therapeutic Modulation by Traditional Chinese Medicine.Drug design, development and therapy · 2026Review
- Decreasing microtubule detyrosination modulates Nav1.5 subcellular distribution and restores sodium current in mdx cardiomyocytes.Cardiovascular research · 2024Article
- Obesity-induced activation of NADPH oxidase 2 prolongs cardiac repolarization via inhibiting K+ currents.PloS one · 2024Article
- Mechanotransduction at the Plasma Membrane-Cytoskeleton Interface.International journal of molecular sciences · 2021Review
- Prevention of connexin-43 remodeling protects against Duchenne muscular dystrophy cardiomyopathy.The Journal of clinical investigation · 2020Article
- Ischemia Enhances the Acute Stretch-Induced Increase in Calcium Spark Rate in Ventricular Myocytes.Frontiers in physiology · 2020Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
key pointsOur group previously discovered and characterized the microtubule mechanotransduction pathway linking diastolic stretch to NADPH oxidase 2-derived reactive oxygen species signals that regulate calcium sparks and calcium influx pathways. Here we used focused experimental tests to constrain and expand our existing computational models of calcium signalling in heart. Mechanistic and quantitative modelling revealed new insights in disease including: changes in microtubule network density and properties, elevated NOX2 expression, altered calcium release dynamics, how NADPH oxidase 2 is activated by and responds to stretch, and finally the degree to which normalizing mechano-activated reactive oxygen species signals can prevent calcium-dependent arrhythmias. ABSTRACT: Microtubule (MT) mechanotransduction links diastolic stretch to generation of NADPH oxidase 2 (NOX2)-dependent reactive oxygen species (ROS), signals we term X-ROS. While stretch-elicited X-ROS primes intracellular calcium (Ca
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