ArticleEMBO molecular medicine2014
The inwardly rectifying K+ channel KIR7.1 controls uterine excitability throughout pregnancy.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 67 citations in OpenAlex.
- Ion Channels as Gatekeepers of Fertility: from Uterine Kir7.1 to Sperm CatSper.Physiology (Bethesda, Md.) · 2027Review
- Bioactive lipid-mediated structural and functional regulation of the essential human potassium channel Kir7.1.Nature communications · 2026Article
- Precision therapeutic tRNA rescue of nonsense mutation R166X inJournal of precision medicine (Amsterdam, Netherlands) · 2025Article
- Myometrial smooth muscle KATP channel activity is attenuated in a mouse model of diet-induced obesity during pregnancy†.Biology of reproduction · 2025Article
- SLO2.1/NALCN Functional Complex Activity in Mouse Myometrial Smooth Muscle Cells During Pregnancy.Journal of cellular physiology · 2025Article
- Kir7.1 is the physiological target for hormones and steroids that regulate uteroplacental function.Science advances · 2025Article
- PUFFFIN: an ultra-bright, customisable, single-plasmid system for labelling cell neighbourhoods.The EMBO journal · 2024Article
- Bitter taste receptors in the reproductive system: Function and therapeutic implications.Journal of cellular physiology · 2024Review
- The unique structural characteristics of the Kir 7.1 inward rectifier potassium channel: a novel player in energy homeostasis control.American journal of physiology. Cell physiology · 2023Review
- Prostaglandin F2α requires activation of calcium-dependent signalling to trigger inflammation in human myometrium.Frontiers in endocrinology · 2023Article
- Article
- Low CLOCK and CRY2 in 2nd trimester human maternal blood and risk of preterm birth: a nested case-control study†.Biology of reproduction · 2021Article
- Next-generation inward rectifier potassium channel modulators: discovery and molecular pharmacology.American journal of physiology. Cell physiology · 2021Review
- Uterine contractions in rodent models and humans.Acta physiologica (Oxford, England) · 2021Review
- Mitochondrial bioenergetic deficits in C9orf72 amyotrophic lateral sclerosis motor neurons cause dysfunctional axonal homeostasis.Acta neuropathologica · 2021Article
- Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications.Handbook of experimental pharmacology · 2021Review
- Enhanced axonal response of mitochondria to demyelination offers neuroprotection: implications for multiple sclerosis.Acta neuropathologica · 2020Article
- A critical role for the inward rectifying potassium channel Kir7.1 in oligodendrocytes of the mouse optic nerve.Brain structure & function · 2020Article
- Drug discovery strategies for the identification of novel regulators of uterine contractility.Current opinion in physiology · 2020Article
- Glial and neuronal expression of the Inward Rectifying Potassium Channel Kir7.1 in the adult mouse brain.Journal of anatomy · 2019Article
Corrections and comments
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Authors and funding
28 authors at 6 institutions in 2 countries.
Funding
Abstract
Abnormal uterine activity in pregnancy causes a range of important clinical disorders, including preterm birth, dysfunctional labour and post-partum haemorrhage. Uterine contractile patterns are controlled by the generation of complex electrical signals at the myometrial smooth muscle plasma membrane. To identify novel targets to treat conditions associated with uterine dysfunction, we undertook a genome-wide screen of potassium channels that are enriched in myometrial smooth muscle. Computational modelling identified Kir7.1 as potentially important in regulating uterine excitability during pregnancy. We demonstrate Kir7.1 current hyper-polarizes uterine myocytes and promotes quiescence during gestation. Labour is associated with a decline, but not loss, of Kir7.1 expression. Knockdown of Kir7.1 by lentiviral expression of miRNA was sufficient to increase uterine contractile force and duration significantly. Conversely, overexpression of Kir7.1 inhibited uterine contractility. Finally, we demonstrate that the Kir7.1 inhibitor VU590 as well as novel derivative compounds induces profound, long-lasting contractions in mouse and human myometrium; the activity of these inhibitors exceeds that of other uterotonic drugs. We conclude Kir7.1 regulates the transition from quiescence to contractions in the pregnant uterus and may be a target for therapies to control uterine contractility.
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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.