ReviewJournal of molecular and cellular cardiology2013
X-ROS signaling in the heart and skeletal muscle: stretch-dependent local ROS regulates [Ca²⁺]i.
Review in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 120 citations in OpenAlex.
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- Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies.Antioxidants (Basel, Switzerland) · 2026Review
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- Inhibition of TRPC3-Nox2 Complex Formation Ameliorates Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2025Article
- Dysferlin and the Regulation of CaCells · 2025Review
- The Heart Is a Smart Pump: Mechanotransduction Mechanisms of the Frank-Starling Law and the Anrep Effect.Annual review of physiology · 2025Review
- Effects of Eleclazine (GS6615) on the proarrhythmic electrophysiological changes induced by myocardial stretch.Frontiers in physiology · 2025Article
- Review
- Acute microtubule changes linked to DMD pathology are insufficient to impair contractile function or enhance contraction-induced injury in healthy muscle.bioRxiv : the preprint server for biology · 2024Article
- Sarcospan Deficiency Increases Oxidative Stress and Arrhythmias in Hearts after Acute Ischemia-Reperfusion Injury.International journal of molecular sciences · 2023Article
- IGFBP1 Sustains Cell Survival during Spatially-Confined Migration and Promotes Tumor Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Detyrosinated microtubule arrays drive myofibrillar malformations inFrontiers in cell and developmental biology · 2023Article
- Growth hormone secretagogues modulate inflammation and fibrosis inFrontiers in immunology · 2023Article
- Actin-microtubule cytoskeletal interplay mediated by MRTF-A/SRF signaling promotes dilated cardiomyopathy caused by LMNA mutations.Nature communications · 2022Article
- Pharmacological TRPC6 inhibition improves survival and muscle function in mice with Duchenne muscular dystrophy.JCI insight · 2022Article
- Modeling cardiomyocyte mechanics and autoregulation of contractility by mechano-chemo-transduction feedback.iScience · 2022Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
X-ROS signaling is a novel redox signaling pathway that links mechanical stress to changes in [Ca(2+)]i. This pathway is activated rapidly and locally within a muscle cell under physiological conditions, but can also contribute to Ca(2+)-dependent arrhythmia in the heart and to the dystrophic phenotype in the heart and skeletal muscle. Upon physiologic cellular stretch, microtubules serve as mechanotransducers to activate NADPH oxidase 2 in the transverse tubules and sarcolemmal membranes to produce reactive oxygen species (ROS). In the heart, the ROS acts locally to activate ryanodine receptor Ca(2+) release channels in the junctional sarcoplasmic reticulum, increasing the Ca(2+) spark rate and "tuning" excitation-contraction coupling. In the skeletal muscle, where Ca(2+) sparks are not normally observed, the X-ROS signaling process is muted. However in muscular dystrophies, such as Duchenne Muscular Dystrophy and dysferlinopathy, X-ROS signaling operates at a high level and contributes to myopathy. Importantly, Ca(2+) permeable stretch-activated channels are activated by X-ROS and contribute to skeletal muscle pathology. Here we review X-ROS signaling and mechanotransduction in striated muscle, and highlight important questions to drive future work on stretch-dependent signaling. We conclude that X-ROS provides an exciting mechanism for the mechanical control of redox and Ca(2+) signaling, but much work is needed to establish its contribution to physiologic and pathophysiologic processes in diverse cell systems.
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Registered trials
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.