ReviewChannels (Austin, Tex.)2014
The bestrophin- and TMEM16A-associated Ca(2+)- activated Cl(–) channels in vascular smooth muscles.
Review in Channels (Austin, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
15 citing papers in PubMed, 29 citations in OpenAlex.
- Loss of Vascular TMEM16A Impairs Cerebral Autoregulation and Exacerbates Ischemia-reperfusion Injury.Translational stroke research · 2026Article
- Acidosis enhances contribution of CaCurrent research in physiology · 2025Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Discovery of Fungus-Derived Nornidulin as a Novel TMEM16A Inhibitor: A Potential Therapy to Inhibit Mucus Secretion in Asthma.Journal of experimental pharmacology · 2023Article
- Chloride Ions, Vascular Function and Hypertension.Biomedicines · 2022Review
- Chloride Channels and Transporters: Roles beyond Classical Cellular Homeostatic pH or Ion Balance in Cancers.Cancers · 2022Review
- Structure and Function of the Bestrophin family of calcium-activated chloride channels.Channels (Austin, Tex.) · 2021Review
- Trophic sympathetic influence weakens pro-contractile role of ClScientific reports · 2020Article
- A paradoxical increase of force development in saphenous and tail arteries from heterozygous ANO1 knockout mice.Physiological reports · 2020Article
- Ion channels and the regulation of myogenic tone in peripheral arterioles.Current topics in membranes · 2020Review
- Elementary calcium signaling in arterial smooth muscle.Channels (Austin, Tex.) · 2019Review
- TMEM16A is implicated in the regulation of coronary flow and is altered in hypertension.British journal of pharmacology · 2019Article
- Ano1 mediates pressure-sensitive contraction frequency changes in mouse lymphatic collecting vessels.The Journal of general physiology · 2019Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Regulation of vascular tone and arterial blood pressure: role of chloride transport in vascular smooth muscle.Pflugers Archiv : European journal of physiology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The presence of Ca(2+)-activated Cl(–) currents (I(Cl(Ca))) in vascular smooth muscle cells (VSMCs) is well established. ICl(Ca) are supposedly important for arterial contraction by linking changes in [Ca(2+)]i and membrane depolarization. Bestrophins and some members of the TMEM16 protein family were recently associated with I(Cl(Ca)). Two distinct I(Cl(Ca)) are characterized in VSMCs; the cGMP-dependent I(Cl(Ca)) dependent upon bestrophin expression and the ‘classical’ Ca(2+)-activated Cl(–) current, which is bestrophin-independent. Interestingly, TMEM16A is essential for both the cGMP-dependent and the classical I(Cl(Ca)). Furthermore, TMEM16A has a role in arterial contraction while bestrophins do not. TMEM16A’s role in the contractile response cannot be explained however only by a simple suppression of the depolarization by Cl(–) channels. It is suggested that TMEM16A expression modulates voltage-gated Ca(2+) influx in a voltage-independent manner and recent studies also demonstrate a complex role of TMEM16A in modulating other membrane proteins.
Indexed as
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.