ReviewAmerican journal of physiology. Cell physiology2012
A network-oriented perspective on cardiac calcium signaling.
Review in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed.
- Immp2l Mutation Induces Mitochondrial Membrane Depolarization and Complex III Activity Suppression after Middle Cerebral Artery Occlusion in Mice.Current medical science · 2023Article
- A multiscale active structural model of the arterial wall accounting for smooth muscle dynamics.Journal of the Royal Society, Interface · 2018Article
- Lipofundin® MCT/LCT 20% increase left ventricular systolic pressure in an ex vivo rat heart model via increase of intracellular calcium level.Korean journal of anesthesiology · 2016Article
- A new system for profiling drug-induced calcium signal perturbation in human embryonic stem cell-derived cardiomyocytes.Journal of biomolecular screening · 2015Article
- A Systemized Approach to Investigate Ca(2+) Synchronization in Clusters of Human Induced Pluripotent Stem-Cell Derived Cardiomyocytes.Frontiers in cell and developmental biology · 2015Article
- Letter to the editor: "Systems biology versus reductionism in cell physiology".American journal of physiology. Cell physiology · 2014Article
- Stimulation of ICa by basal PKA activity is facilitated by caveolin-3 in cardiac ventricular myocytes.Journal of molecular and cellular cardiology · 2014Article
- Interference with ERK(Thr188) phosphorylation impairs pathological but not physiological cardiac hypertrophy.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
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.
Funding
Abstract
The normal contractile, electrical, and energetic function of the heart depends on the synchronization of biological oscillators and signal integrators that make up cellular signaling networks. In this review we interpret experimental data from molecular, cellular, and transgenic models of cardiac signaling behavior in the context of established concepts in cell network architecture and organization. Focusing on the cellular Ca(2+) handling machinery, we describe how the plasticity and adaptability of normal Ca(2+) signaling is dependent on dynamic network configurations that operate across a wide range of functional states. We consider how (mal)adaptive changes in signaling pathways restrict the dynamic range of the network such that it cannot respond appropriately to physiologic stimuli or perturbation. Based on these concepts, a model is proposed in which pathologic abnormalities in cardiac rhythm and contractility (e.g., arrhythmias and heart failure) arise as a consequence of progressive desynchronization and reduction in the dynamic range of the Ca(2+) signaling network. We discuss how a systems-level understanding of the network organization, cellular noise, and chaotic behavior may inform the design of new therapeutic modalities that prevent or reverse the disease-linked unraveling of the Ca(2+) signaling network.
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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.