ReviewJournal of molecular and cellular cardiology2009
Molecular and biophysical mechanisms of Ca2+ sparklets in smooth muscle.
Review in Journal of molecular and cellular cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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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
25 citing papers in PubMed, 42 citations in OpenAlex.
- Sequential Gating of Ryanodine Receptors Underlies the Development of Calcium Sparks in Frog Skeletal Muscle.Biomolecules · 2026Article
- Sorbs2 Modulation of BK Channels in Arterial Myocytes: Implications for Diabetes.Circulation research · 2024Article
- Mechanisms and physiological implications of cooperative gating of clustered ion channels.Physiological reviews · 2022Review
- Functional tuning of Vascular L-type CaFrontiers in physiology · 2022Review
- Calcium signals that determine vascular resistance.Wiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Gene Expressions Underlying Mishandled Calcium Clearance and Elevated Generation of Reactive Oxygen Species in the Coronary Artery Smooth Muscle Cells of Chronic Heart Failure Rats.Chinese medical journal · 2017Article
- Calcium Channels in Vascular Smooth Muscle.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Membrane potential and Ca2+ concentration dependence on pressure and vasoactive agents in arterial smooth muscle: A model.The Journal of general physiology · 2015Article
- Vascular TRP channels: performing under pressure and going with the flow.Physiology (Bethesda, Md.) · 2014Review
- Detection of differentially regulated subsarcolemmal calcium signals activated by vasoactive agonists in rat pulmonary artery smooth muscle cells.American journal of physiology. Cell physiology · 2014Article
- Caveolin-1 facilitates the direct coupling between large conductance Ca2+-activated K+ (BKCa) and Cav1.2 Ca2+ channels and their clustering to regulate membrane excitability in vascular myocytes.The Journal of biological chemistry · 2013Article
- Down-regulation of CaV1.2 channels during hypertension: how fewer CaV1.2 channels allow more Ca(2+) into hypertensive arterial smooth muscle.The Journal of physiology · 2013Article
- Capturing single L-type Ca(2+) channel function with optics.Biochimica et biophysica acta · 2013Review
- CaV1.2 sparklets in heart and vascular smooth muscle.Journal of molecular and cellular cardiology · 2013Review
- Calcium dynamics in vascular smooth muscle.Microcirculation (New York, N.Y. : 1994) · 2013Review
- Local regulation of L-type Ca²⁺ channel sparklets in arterial smooth muscle.Microcirculation (New York, N.Y. : 1994) · 2013Review
- Tonic and phasic smooth muscle contraction is not regulated by the PKCα - CPI-17 pathway in swine stomach antrum and fundus.PloS one · 2013Article
- Hydrogen sulfide activates Ca²⁺ sparks to induce cerebral arteriole dilatation.The Journal of physiology · 2012Article
- Endogenous cytosolic Ca(2+) buffering is necessary for TRPM4 activity in cerebral artery smooth muscle cells.Cell calcium · 2012Article
- Calcium signaling in smooth muscle.Cold Spring Harbor perspectives in biology · 2011Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In this article, we review the biophysical basis and functional implications of a novel Ca(2+) signal (called "Ca(2+) sparklets") produced by Ca(2+) influx via L-type Ca(2+) channels (LTCCs) in smooth muscle. Ca(2+) sparklet activity is bimodal. In low activity mode, Ca(2+) sparklets are produced by random, brief openings of solitary LTCCs. In contrast, small clusters of LTCCs can function in a high activity mode that creates sites of continual Ca(2+) influx called "persistent Ca(2+) sparklets". Low activity and persistent Ca(2+) sparklets contribute to Ca(2+) influx in arterial, colonic, and venous smooth muscle. Targeting of PKCalpha by the scaffolding protein AKAP150 to specific sarcolemmal domains is required for the activation of persistent Ca(2+) sparklets. Calcineurin, which is also associated with AKAP150, opposes the actions of PKCalpha on Ca(2+) sparklets. At hyperpolarized potentials, Ca(2+) sparklet activity is low and hence does not contribute to global [Ca(2+)](i). Membrane depolarization increases low and persistent Ca(2+) sparklet activity, thereby increasing local and global [Ca(2+)](i). Ca(2+) sparklet activity is increased in arterial myocytes during hypertension, thus increasing Ca(2+) influx and activating the transcription factor NFATc3. We discuss a model for subcellular variations in Ca(2+) sparklet activity and their role in the regulation of excitation-contraction coupling and excitation-transcription coupling in smooth muscle.
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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.