ReviewFrontiers in pharmacology2015
Ca(2+) signaling in the myocardium by (redox) regulation of PKA/CaMKII.
Review in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 36 citations in OpenAlex.
- A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026Article
- ROS accelerates the progression of hypertrophic cardiomyopathy.Genes & diseases · 2026Article
- Multifaceted Impact of SGLT2 Inhibitors in Heart Failure Patients: Exploring Diverse Mechanisms of Action.Biomedicines · 2024Review
- Mitochondrial Dysfunction in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Redox Modification of PKA-Cα Differentially Affects Its Substrate Selection.Life (Basel, Switzerland) · 2023Article
- Changes of energy metabolism in failing heart and its regulation by SIRT3.Heart failure reviews · 2023Review
- Multi-omics approaches for comprehensive analysis and understanding of the immune response in the miniature pig breed.PloS one · 2022Article
- Attenuating persistent sodium current-induced atrial myopathy and fibrillation by preventing mitochondrial oxidative stress.JCI insight · 2021Article
- Uncovering sex-specific mechanisms of action of testosterone and redox balance.Redox biology · 2020Review
- Screening forTheranostics · 2020Article
- Degradation of GRK2 and AKT is an early and detrimental event in myocardial ischemia/reperfusion.EBioMedicine · 2019Article
- Nox1/Ref-1-mediated activation of CREB promotes Gremlin1-driven endothelial cell proliferation and migration.Redox biology · 2019Article
- Physiological and unappreciated roles of CaMKII in the heart.Basic research in cardiology · 2018Review
- Silibinin sensitizes TRAIL-mediated apoptosis by upregulating DR5 through ROS-induced endoplasmic reticulum stress-CaOncotarget · 2018Article
- Redox Dependent Modifications of Ryanodine Receptor: Basic Mechanisms and Implications in Heart Diseases.Frontiers in physiology · 2018Review
- The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited.Oxidative medicine and cellular longevity · 2016Review
- Tolerance to nascent protein misfolding stress requires fine-tuning of the cAMP/PKA pathway.The Journal of biological chemistryArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Homeostatic cardiac function is maintained by a complex network of interdependent signaling pathways which become compromised during disease progression. Excitation-contraction-coupling, the translation of an electrical signal to a contractile response is critically dependent on a tightly controlled sequence of events culminating in a rise in intracellular Ca(2+) and subsequent contraction of the myocardium. Dysregulation of this Ca(2+) handling system as well as increases in the production of reactive oxygen species (ROS) are two major contributing factors to myocardial disease progression. ROS, generated by cellular oxidases and by-products of cellular metabolism, are highly reactive oxygen derivatives that function as key secondary messengers within the heart and contribute to normal homeostatic function. However, excessive production of ROS, as in disease, can directly interact with kinases critical for Ca(2+) regulation. This post-translational oxidative modification therefore links changes in the redox status of the myocardium to phospho-regulated pathways essential for its function. This review aims to describe the oxidative regulation of the Ca(2+)/calmodulin-dependent kinase II (CaMKII) and cAMP-dependent protein kinase A (PKA), and the subsequent impact this has on Ca(2+) handling within the myocardium. Elucidating the impact of alterations in intracellular ROS production on Ca(2+) dynamics through oxidative modification of key ROS sensing kinases, may provide novel therapeutic targets for preventing myocardial disease progression.
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Identifiers
What OpenQuestion holds
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.