ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016
Kcne4 deletion sex- and age-specifically impairs cardiac repolarization in mice.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- KCNE gene family: From basic functions to diseases.Genes & diseases · 2026Review
- Functions of the KCNE Gene Family in Ion Channels.Biochemical genetics · 2026Review
- Voltage-dependent potassium channel regulatory subunits in the immune system.Biophysical reviews · 2026Review
- Dose-dependent exercise promotes the transition from atrial protection to arrhythmogenic vulnerability: the intermediary role of calcium handling instability in substrate remodeling.Frontiers in physiology · 2026Article
- Cycling matters: Sex hormone regulation of vascular potassium channels.Channels (Austin, Tex.) · 2023Review
- Intrapericardial long non-coding RNA-Tcf21 antisense RNA inducing demethylation administration promotes cardiac repair.European heart journal · 2023Article
- Kv Channel Ancillary Subunits: Where Do We Go from Here?Physiology (Bethesda, Md.) · 2022Review
- Induction of potassium channel regulator KCNE4 in a submandibular lymph node metastasis model.Scientific reports · 2022Article
- Deletion in mice of X-linked, Brugada syndrome- and atrial fibrillation-associated Kcne5 augments ventricular KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Deconstruction of an African folk medicine uncovers a novel molecular strategy for therapeutic potassium channel activation.Science advances · 2018Article
- Kcne4 deletion sex-specifically predisposes to cardiac arrhythmia via testosterone-dependent impairment of RISK/SAFE pathway induction in aged mice.Scientific reports · 2018Article
- Prenatal androgen exposure causes hypertension and gut microbiota dysbiosis.Gut microbes · 2018Article
- Heteromeric complexes of aldo-keto reductase auxiliary KChemico-biological interactions · 2017Article
- Regulation of human cardiac potassium channels by full-length KCNE3 and KCNE4.Scientific reports · 2016Article
- Review
- The C-terminal domain of Kv1.3 regulates functional interactions with the KCNE4 subunit.Journal of cell science · 2016Article
- Novel exon 1 protein-coding regions N-terminally extend human KCNE3 and KCNE4.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Kcne2 deletion attenuates acute post-ischaemia/reperfusion myocardial infarction.Cardiovascular research · 2016Article
- Kcne4 Deletion Sex-Dependently Alters Vascular Reactivity.Journal of vascular research · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Myocardial repolarization capacity varies with sex, age, and pathology; the molecular basis for this variation is incompletely understood. Here, we show that the transcript for KCNE4, a voltage-gated potassium (Kv) channel β subunit associated with human atrial fibrillation, was 8-fold more highly expressed in the male left ventricle compared with females in young adult C57BL/6 mice (P < 0.05). Similarly, Kv current density was 25% greater in ventricular myocytes from young adult males (P < 0.05). Germ-line Kcne4 deletion eliminated the sex-specific Kv current disparity by diminishing ventricular fast transient outward current (Ito,f) and slowly activating K(+) current (IK,slow1). Kcne4 deletion also reduced Kv currents in male mouse atrial myocytes, by >45% (P < 0.001). As we previously found for Kv4.2 (which generates mouse Ito,f), heterologously expressed KCNE4 functionally regulated Kv1.5 (the Kv α subunit that generates IKslow1 in mice). Of note, in postmenopausal female mice, ventricular repolarization was impaired by Kcne4 deletion, and ventricular Kcne4 expression increased to match that of males. Moreover, castration diminished male ventricular Kcne4 expression 2.8-fold, whereas 5α-dihydrotestosterone (DHT) implants in castrated mice increased Kcne4 expression >3-fold (P = 0.01) to match noncastrated levels. KCNE4 is thereby shown to be a DHT-regulated determinant of cardiac excitability and a molecular substrate for sex- and age-dependent cardiac arrhythmogenesis.
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Registered trials
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