ReviewPflugers Archiv : European journal of physiology2008
The non-excitable smooth muscle: calcium signaling and phenotypic switching during vascular disease.
Review in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 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
133 citing papers in PubMed, 252 citations in OpenAlex.
- Uncovering a Sex-Specific cAMP Landscape in Vascular Smooth Muscle.bioRxiv : the preprint server for biology · 2026Article
- CaThe Journal of physiology · 2026Article
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- The Correlation Between Plasma CACNA2D1 Protein Concentration and the Severity of Coronary Heart Disease.Journal of cardiovascular development and disease · 2026Article
- Intron polymorphism in Camk2d is associated with ventricular arrhythmias in normal adult Sprague-Dawley rats.Experimental animals · 2026Article
- KPharmaceuticals (Basel, Switzerland) · 2026Review
- Arterial Myocyte Pannexin 1 Channel Controls Vascular Reactivity in Diabetic Hyperglycemia.Circulation research · 2025Article
- Orphan Under Pressure: GPR146 as a Mechanotransduction Modulator.Circulation research · 2025Article
- The Pathophysiological Role of Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysm.Cells · 2025Review
- DAPK1 acts as a positive regulator of hypertension via induction of vasoconstriction.Clinical science (London, England : 1979) · 2025Article
- Vessel-On-A-Chip Coupled Proteomics Reveal Pressure-Overload-Induced Vascular Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identifying and validating hypoxia- and metabolism-related hub genes and cell communication in atherosclerosis.Frontiers in cardiovascular medicine · 2025Article
- Protective effect of SERCA2a-SUMOylation by SUMO-1 on diabetes-induced atherosclerosis and aortic vascular injury.Molecular and cellular biochemistry · 2025Article
- Role for the PIPJournal of cell communication and signaling · 2024Review
- Inositol 1,4,5-Trisphosphate Receptors Regulate Vascular Smooth Muscle Cell Proliferation and Neointima Formation in Mice.Journal of the American Heart Association · 2024Article
- Vascular polycystin proteins in health and disease.Microcirculation (New York, N.Y. : 1994) · 2024Review
- Cardiovascular perspectives of the TRP channel polycystin 2.The Journal of physiology · 2024Article
- The Reappraisal of the Reappraisal-CRAC Channels Are Activated by L-Type CaFunction (Oxford, England) · 2024Article
- Direct modulation of TRPC ion channels by Gα proteins.Frontiers in physiology · 2024Review
- Gastrodin attenuates angiotensin II-induced vascular contraction and MLCK/p-MLCPharmaceutical biology · 2023Article
73 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Calcium (Ca(2+)) is a highly versatile second messenger that controls vascular smooth muscle cell (VSMC) contraction, proliferation, and migration. By means of Ca(2+) permeable channels, Ca(2+) pumps and channels conducting other ions such as potassium and chloride, VSMC keep intracellular Ca(2+) levels under tight control. In healthy quiescent contractile VSMC, two important components of the Ca(2+) signaling pathways that regulate VSMC contraction are the plasma membrane voltage-operated Ca(2+) channel of the high voltage-activated type (L-type) and the sarcoplasmic reticulum Ca(2+) release channel, Ryanodine Receptor (RyR). Injury to the vessel wall is accompanied by VSMC phenotype switch from a contractile quiescent to a proliferative motile phenotype (synthetic phenotype) and by alteration of many components of VSMC Ca(2+) signaling pathways. Specifically, this switch that culminates in a VSMC phenotype reminiscent of a non-excitable cell is characterized by loss of L-type channels expression and increased expression of the low voltage-activated (T-type) Ca(2+) channels and the canonical transient receptor potential (TRPC) channels. The expression levels of intracellular Ca(2+) release channels, pumps and Ca(2+)-activated proteins are also altered: the proliferative VSMC lose the RyR3 and the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase isoform 2a pump and reciprocally regulate isoforms of the ca(2+)/calmodulin-dependent protein kinase II. This review focuses on the changes in expression of Ca(2+) signaling proteins associated with VSMC proliferation both in vitro and in vivo. The physiological implications of the altered expression of these Ca(2+) signaling molecules, their contribution to VSMC dysfunction during vascular disease and their potential as targets for drug therapy will be discussed.
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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.