ArticleFASEB bioAdvances2020
Potentiating TMEM16A does not stimulate airway mucus secretion or bronchial and pulmonary arterial smooth muscle contraction.
Article in FASEB bioAdvances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 34 citations in OpenAlex.
- Randomized, phase I studies to evaluate the safety, tolerability, and pharmacokinetics of an inhaled, TMEM16A potentiator, GDC-6988, in healthy subjects.Therapeutic advances in respiratory diseaseTrial
- Natural Products Targeting Airway Inflammation and Mucus Hypersecretion: Molecular Mechanisms and Therapeutic Potential for Respiratory Health.Nutrients · 2026Review
- Qualitative beta-2-adrenoceptor signaling in the regulation of human airway epithelia mucin and cytokine production.Respiratory research · 2026Article
- Airway mucus in infection.Frontiers in physiology · 2026Review
- Restoring chloride efflux in cystic fibrosis with TMEM16a antisense oligonucleotides.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- TMEM16 proteins: CaInternational journal of molecular medicine · 2024Review
- Cystic fibrosis.Nature reviews. Disease primers · 2024Review
- Niclosamide potentiates TMEM16A and induces vasoconstriction.The Journal of general physiology · 2024Article
- CaInternational journal of molecular sciences · 2024Review
- Function and Regulation of the Calcium-Activated Chloride Channel Anoctamin 1 (TMEM16A).Handbook of experimental pharmacology · 2024Article
- Red ginseng aqueous extract improves mucociliary transport dysfunction and histopathology in CF rat airways.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2023Article
- Niclosamide does not modulate airway epithelial function through blocking of the calcium activated chloride channel, TMEM16A.Frontiers in pharmacology · 2023Article
- Role of ANO1 in tumors and tumor immunity.Journal of cancer research and clinical oncology · 2022Review
- Reduced Expression of TMEM16A Impairs Nitric Oxide-Dependent ClFrontiers in cellular neuroscience · 2022Article
- Chloride transport modulators as drug candidates.American journal of physiology. Cell physiology · 2021Review
- Human Molecular Genetics and the long road to treating cystic fibrosis.Human molecular genetics · 2021Review
- Cross-talk of inflammatory mediators and airway epithelium reveals the cystic fibrosis transmembrane conductance regulator as a major target.ERJ open research · 2021Article
- Mucus Release and Airway Constriction by TMEM16A May Worsen Pathology in Inflammatory Lung Disease.International journal of molecular sciences · 2021Article
- Review
- Pharmacological Modulation of Ion Channels for the Treatment of Cystic Fibrosis.Journal of experimental pharmacology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
The calcium-activated chloride channel (CaCC) TMEM16A enables chloride secretion across several transporting epithelia, including in the airways. Additional roles for TMEM16A have been proposed, which include regulating mucus production and secretion and stimulating smooth muscle contraction. The aim of the present study was to test whether the pharmacological regulation of TMEM16A channel function, could affect any of these proposed biological roles in the airways. In vitro, neither a potent and selective TMEM16A potentiator (ETX001) nor the potent TMEM16A inhibitor (Ani9) influenced either baseline mucin release or goblet cell numbers in well-differentiated primary human bronchial epithelial (HBE) cells. In vivo, a TMEM16A potentiator was without effect on goblet cell emptying in an IL-13 stimulated goblet cell metaplasia model. Using freshly isolated human bronchi and pulmonary arteries, neither ETX001 or Ani9 had any effect on the contractile or relaxant responses of the tissues. In vivo, ETX001 also failed to influence either lung or cardiovascular function when delivered directly into the airways of telemetered rats. Together, these studies do not support a role for TMEM16A in the regulation of goblet cell numbers or baseline mucin release, or on the regulation of airway or pulmonary artery smooth muscle contraction.
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.