ArticleBritish journal of pharmacology2019
TMEM16A is implicated in the regulation of coronary flow and is altered in hypertension.
Article in British journal of pharmacology, 2019. 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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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Loss of Vascular TMEM16A Impairs Cerebral Autoregulation and Exacerbates Ischemia-reperfusion Injury.Translational stroke research · 2026Article
- CaActa physiologica (Oxford, England) · 2026Review
- TMEM16A channel signalling microdomains in the regulation of vascular function.The Journal of physiology · 2026Review
- TMEM16A in gastrointestinal and vascular smooth muscle contractility.The Journal of physiology · 2025Review
- The machinery of healthy vasodilatation: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- The emerging role of anoctamin-1 in cardiac and cerebrovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- ANO1: central role and clinical significance in non-neoplastic and neoplastic diseases.Frontiers in immunology · 2025Review
- Acidosis enhances contribution of CaCurrent research in physiology · 2025Article
- Distinct modulation of calcium-activated chloride channel TMEM16A by drug-binding sites.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- ANO1, CaV1.2, and IP3R form a localized unit of EC-coupling in mouse pulmonary arterial smooth muscle.The Journal of general physiology · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Marked oestrous cycle-dependent regulation of rat arterial KBritish journal of pharmacology · 2023Article
- Hepatocyte-specific TMEM16A deficiency alleviates hepatic ischemia/reperfusion injury via suppressing GPX4-mediated ferroptosis.Cell death & disease · 2022Article
- Chloride Ions, Vascular Function and Hypertension.Biomedicines · 2022Review
- Clues and new evidences in arterial hypertension: unmasking the role of the chloride anion.Pflugers Archiv : European journal of physiology · 2022Review
- A small molecule inhibitor of the chloride channel TMEM16A blocks vascular smooth muscle contraction and lowers blood pressure in spontaneously hypertensive rats.Kidney international · 2021Article
- The CaActa pharmaceutica Sinica. B · 2021Review
- TMEM16A channel upregulation in arterial smooth muscle cells produces vasoconstriction during diabetes.American journal of physiology. Heart and circulatory physiology · 2021Article
- 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
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposeCoronary artery disease leads to ischaemic heart disease and ultimately myocardial infarction. Thus, it is important to determine the factors that regulate coronary blood flow. Ca EXPERIMENTAL APPROACH: We performed mRNA and protein analysis, electrophysiological studies of coronary artery myocytes, and functional studies of coronary artery contractility and coronary perfusion, using novel inhibitors of TMEM16A. Furthermore, we assessed whether any changes in expression and function occurred in coronary arteries from spontaneously hypertensive rats (SHRs). KEY
resultsTMEM16A was expressed in rat coronary arteries. The TMEM16A-specific inhibitor, MONNA, hyperpolarised the membrane potential in U46619. MONNA, T16A CONCLUSIONS AND IMPLICATIONS: In conclusion, TMEM16A is a key regulator of coronary blood flow and is implicated in the altered contractility of coronary arteries from SHRs.
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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.