ReviewAntioxidants & redox signaling2013
Redox regulation of sodium and calcium handling.
Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.
- The role of the PM2.5-associated metals in pathogenesis of child Mycoplasma Pneumoniae infections: a systematic review.Environmental science and pollution research international · 2016Pooled it
- A quantitative redox proteome of the human muscle response to exercise.bioRxiv : the preprint server for biology · 2026Article
- The Sirt3-CD38 axis induces mitochondrial dysfunction in hypertrophied heart by regulating mitochondrial calcium overload.European journal of medical research · 2025Article
- Exercise Empowerment: A Multifaceted Anatomy in Managing Diabetic Myocardial Disorder.Journal of cardiovascular translational research · 2025Review
- The Association Between Oxidative Stress and the Progression of Heart Failure: A Systematic Review.Cureus · 2024Review
- The inotropic and arrhythmogenic effects of acutely increased late IFrontiers in cardiovascular medicine · 2024Article
- Nongenetic Optical Modulation of Pluripotent Stem Cells Derived Cardiomyocytes Function in the Red Spectral Range.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mitochondrial Calcium Overload Plays a Causal Role in Oxidative Stress in the Failing Heart.Biomolecules · 2023Review
- Mechano-energetic uncoupling in hypertrophic cardiomyopathy: Pathophysiological mechanisms and therapeutic opportunities.Journal of molecular and cellular cardiology plus · 2023Review
- Flipping Off and On the Redox Switch in the Microcirculation.Annual review of physiology · 2023Review
- Glymphatic Dysfunction Induced Oxidative Stress and Neuro-Inflammation in Major Depression Disorders.Antioxidants (Basel, Switzerland) · 2022Review
- Citrullination is linked to reduced CaActa physiologica (Oxford, England) · 2022Article
- Cardioprotective Antioxidant and Anti-Inflammatory Mechanisms Induced by Intermittent Hypobaric Hypoxia.Antioxidants (Basel, Switzerland) · 2022Article
- Mitochondrial Fusion, Fission, and Mitophagy in Cardiac Diseases: Challenges and Therapeutic Opportunities.Antioxidants & redox signaling · 2022Review
- Enhanced Cardiac CaMKII Oxidation and CaMKII-Dependent SR Ca Leak in Patients with Sleep-Disordered Breathing.Antioxidants (Basel, Switzerland) · 2022Article
- Benefits of SGLT2 inhibitors in arrhythmias.Frontiers in cardiovascular medicine · 2022Review
- Pinocembrin Decreases Atrial Fibrillation Susceptibility in a Rodent Model of Depression.Frontiers in cardiovascular medicine · 2022Article
- Calcium dysregulation increases right ventricular outflow tract arrhythmogenesis in rabbit model of chronic kidney disease.Journal of cellular and molecular medicine · 2021Article
- Angiotensin receptor-neprilysin inhibition by sacubitril/valsartan attenuates doxorubicin-induced cardiotoxicity in a pretreatment mice model by interfering with oxidative stress, inflammation, and Caspase 3 apoptotic pathway.Anatolian journal of cardiology · 2021Article
- Enhanced Heart Failure in Redox-Dead Cys17Ser PKARIα Knock-In Mice.Journal of the American Heart Association · 2021Article
24 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
significanceIn heart failure (HF), contractile dysfunction and arrhythmias result from disturbed intracellular Ca handling. Activated stress kinases like cAMP-dependent protein kinase A (PKA), protein kinase C (PKC), and Ca/calmodulin-dependent protein kinase II (CaMKII), which are known to influence many Ca-regulatory proteins, are mechanistically involved. RECENT ADVANCES: Beside classical activation pathways, it is becoming increasingly evident that reactive oxygen species (ROS) can directly oxidize these kinases, leading to alternative activation. Since HF is associated with increased ROS generation, ROS-activated serine/threonine kinases may play a crucial role in the disturbance of cellular Ca homeostasis. Many of the previously described ROS effects on ion channels and transporters are possibly mediated by these stress kinases. For instance, ROS have been shown to oxidize and activate CaMKII, thereby increasing Na influx through voltage-gated Na channels, which can lead to intracellular Na accumulation and action potential prolongation. Consequently, Ca entry via activated NCX is favored, which together with ROS-induced dysfunction of the sarcoplasmic reticulum can lead to dramatic intracellular Ca accumulation, diminished contractility, and arrhythmias. CRITICAL ISSUES: While low amounts of ROS may regulate kinase activity, excessive uncontrolled ROS production may lead to direct redox modification of Ca handling proteins. Therefore, depending on the source and amount of ROS generated, ROS could have very different effects on Ca-handling proteins. FUTURE DIRECTIONS: The discrimination between fine-tuned ROS signaling and unspecific ROS damage may be crucial for the understanding of heart failure development and important for the investigation of targeted treatment strategies.
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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.