ArticleScientific reports2018
Kcne4 deletion sex-specifically predisposes to cardiac arrhythmia via testosterone-dependent impairment of RISK/SAFE pathway induction in aged mice.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Association between blood cobalt ion concentrations and anemia and cardiovascular diseases: novel evidence of toxicity resulting from metal implants.Frontiers in nutrition · 2025Article
- Identification of KCNE6, a new member of the KCNE family of potassium channel auxiliary subunits.Communications biology · 2024Article
- Potassium voltage‑gated channel subfamily E member 4 facilitates the malignant progression of colon cancer by enhancing EGF containing fibulin extracellular matrix protein 2 expression.Experimental and therapeutic medicine · 2023Article
- Kv Channel Ancillary Subunits: Where Do We Go from Here?Physiology (Bethesda, Md.) · 2022Review
- Potential Therapies to Protect the Aging Heart Against Ischemia/Reperfusion Injury.Frontiers in cardiovascular medicine · 2021Review
- 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
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5 authors.
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Abstract
Sudden cardiac death (SCD) is associated with both electrical and ischemic substrates, and is a major cause of ischemic heart disease mortality worldwide. Male sex predisposes to SCD but the underlying mechanisms are incompletely understood. KCNE4, a cardiac arrhythmia-associated potassium channel β-subunit, is upregulated by 5α-dihydrotestosterone (DHT). Thus, ventricular Kcne4 expression is low in young adult female mice, but high in males and postmenopausal (12+ months) females. Despite causing a sex-independent electrical substrate at 13 months of age (22% QT prolongation in both males and females; P < 0.01), Kcne4 deletion preferentially predisposed aged male mice to ischemia/reperfusion (IR)-provoked ventricular tachyarrhythmias. Interestingly, Kcne4 deletion caused baseline induction of cardioprotective RISK and SAFE pathways in 13-m-old female, but not male, mice. IR-invoked RISK/SAFE induction was also deficient in male but not female Kcne4
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