ReviewJournal of molecular and cellular cardiology2008
Ca2+ clearance and contractility in vascular smooth muscle: evidence from gene-altered murine models.
Review in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- Vascular dysfunction caused by loss of Brn-3b/POU4F2 transcription factor in aortic vascular smooth muscle cells is linked to deregulation of calcium signalling pathways.Cell death & disease · 2023Article
- Propulsive colonic contractions are mediated by inhibition-driven poststimulus responses that originate in interstitial cells of Cajal.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Elucidation of Cellular Mechanisms That Regulate the Sustained Contraction and Relaxation of the Mammalian Iris.Investigative ophthalmology & visual science · 2020Article
- Divergent modification of low-dose ⁵⁶Fe-particle and proton radiation on skeletal muscle.Radiation research · 2013Article
- Transcriptome analysis for Notch3 target genes identifies Grip2 as a novel regulator of myogenic response in the cerebrovasculature.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Silencing MaxiK activity in corporal smooth muscle cells initiates compensatory mechanisms to maintain calcium homeostasis.The journal of sexual medicine · 2011Article
- Regulation of gastrointestinal motility by Ca2+/calmodulin-stimulated protein kinase II.Archives of biochemistry and biophysics · 2011Review
- Mechanism of glucose-6-phosphate dehydrogenase-mediated regulation of coronary artery contractility.American journal of physiology. Heart and circulatory physiology · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The central importance of calcium clearance proteins, and their regulators, in the modulation of myocardial contractility and intracellular Ca(2+) concentration ([Ca(2+)](i)) has long been established. Key players identified include the Na(+)-Ca(2+) exchanger, the Na(+)-K(+) ATPase, the sarco(endo)plasmic reticulum Ca(2+)-ATPase and associated phospholamban. Gene-targeted and transgenic murine models have been critical in the elucidation of their function. The study of these proteins in the regulation of contractile parameters in vascular smooth muscle, on the other hand, is less well studied. More recently, gene-targeted and transgenic models have expanded our knowledge of Ca(2+) clearance proteins and their role in both tonic and phasic smooth muscle contractility. In this review, we will briefly treat the mechanisms which underlie Ca(2+) clearance in smooth muscle. These will be addressed in light of studies using gene-modified mouse models, the results of which will be compared and contrasted with those in the cardiomyocyte. The recently identified human mutations in phospholamban, which lead to dilated cardiomyopathy, are also present in vascular and other smooth muscle. Given the importance of these Ca(2+) clearance systems to modulation of smooth muscle, it is likely that mutations will also lead to smooth muscle pathology.
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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.