ReviewExpert opinion on therapeutic targets2010
Vascular KCa-channels as therapeutic targets in hypertension and restenosis disease.
Review in Expert opinion on therapeutic targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 84 citations in OpenAlex.
- Carbon dioxide is a triple vasodilator.Cardiovascular research · 2026Article
- The KCa3.1 KCells · 2026Review
- Prognostic Factors for In-stent Restenosis After Cerebrovascular Stent Implantation among Ischemic Stroke Patients.Current neurovascular research · 2026Article
- Genetic silencing of KChannels (Austin, Tex.) · 2025Article
- Apitherapy combination improvement of blood pressure, cardiovascular protection, and antioxidant and anti-inflammatory responses in dexamethasone model hypertensive rats.Scientific reports · 2022Article
- The Potential Role of Everlasting Flower (Antioxidants (Basel, Switzerland) · 2022Article
- Role of SNARE Proteins in the Insertion of KCa3.1 in the Plasma Membrane of a Polarized Epithelium.Frontiers in physiology · 2022Article
- Hydrophobic interactions between the HA helix and S4-S5 linker modulate apparent CaActa physiologica (Oxford, England) · 2021Article
- Mechanisms underlying selective coupling of endothelial CaThe Journal of physiology · 2020Article
- Article
- De novo loss-of-function KCNMA1 variants are associated with a new multiple malformation syndrome and a broad spectrum of developmental and neurological phenotypes.Human molecular genetics · 2019Article
- Modulation of Cardiovascular Function in Primary Hypertension in Rat by SKA-31, an Activator ofInternational journal of molecular sciences · 2019Article
- Royal jelly causes hypotension and vasodilation induced by increasing nitric oxide production.Food science & nutrition · 2019Article
- Article
- Pu-Erh Tea Relaxes the Thoracic Aorta of Rats by Reducing Intracellular Calcium.Frontiers in pharmacology · 2019Article
- Propofol-induced vasodilation of mesenteric arterioles via BKExperimental and therapeutic medicine · 2018Article
- Pharmacologic targeting of endothelial CaChannels (Austin, Tex.) · 2018Review
- Plasma membrane insertion of KCa2.3 (SK3) is dependent upon the SNARE proteins, syntaxin-4 and SNAP23.PloS one · 2018Article
- The KCa3.1 blocker TRAM34 reverses renal damage in a mouse model of established diabetic nephropathy.PloS one · 2018Article
- Structural insights into the potency of SK channel positive modulators.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
importance of the fieldCardiovascular disease is a leading cause of death in modern societies. Hyperpolarizing Ca(2+)-activated K(+) channels (K(Ca)) are important membrane proteins in the control of arterial tone and pathological vascular remodelling and thus could serve as new drug targets. AREAS COVERED IN THIS REVIEW: We summarize recent advances in the field of vascular K(Ca) and their roles in cardiovascular pathologies such as hypertension and restenosis disease and draw attention to novel small-molecule channel modulators and their possible therapeutic utility. This review focuses on literature from the last four to five years. WHAT THE READER WILL GAIN: Pharmacological opening of endothelial KCa3.1/KCa2.3 channels stimulates endothelium-derived-hyperpolarizing-factor-mediated arteriolar dilation and lowers blood pressure. Inhibition of smooth muscle KCa3.1 channels has beneficial effects in restenosis disease and atherosclerosis. We consider the therapeutic potential of KCa3.1/KCa2.3 openers as novel endothelium-specific antihypertensive drugs as well as of KCa3.1-blockers for the treatment of pathological vascular remodelling and discuss advantages and disadvantages of the pharmacotherapeutic approaches. TAKE HOME MESSAGE: Pharmacological manipulation of vascular K(Ca) channels by novel small-molecule modulators offers new venues for alternative treatments of hypertension, restenosis and atherosclerosis. Additional efforts are required to optimize these compounds and to validate them as cardiovascular-protective drugs.
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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.