|
Sick Sinus Syndrome
|
0.440 |
AlteredExpression
|
disease |
BEFREE |
This study is to investigate how mitochondrial oxidative stress induces HCN4 downregulation associated with in sick sinus syndrome.
|
31751569 |
2020 |
|
Atrial Fibrillation
|
0.490 |
GeneticVariation
|
disease |
BEFREE |
Together with the common KCNE1 variant S38G, previously proposed as a genetic modifier of AF, HCN4-P883R may provide a substrate for the development of AF and TIC.
|
31481236 |
2019 |
|
Atrial Fibrillation
|
0.490 |
Biomarker
|
disease |
BEFREE |
In this review, we summarize the current knowledge of the HCN4 channel and ivabradine, including the function of HCN4 in cardiac pacemaking, the mechanism of action of I<sub>f</sub> inhibition by ivabradine, and the pharmacological and clinical effects of ivabradine in cardiac diseases as HF, coronary artery disease, and atrial fibrillation.
|
30606942 |
2019 |
|
Brugada Syndrome (disorder)
|
0.320 |
GeneticVariation
|
disease |
BEFREE |
In the present study, the potential correlation between HCN4 gene variations and the occurrence of SUNDS was investigated.
|
30452770 |
2019 |
|
Waist-Hip Ratio
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Meta-analysis of genome-wide association studies for body fat distribution in 694 649 individuals of European ancestry.
|
30239722 |
2019 |
|
Cardiac Arrhythmia
|
0.080 |
GeneticVariation
|
phenotype |
BEFREE |
Mutations of genes specific for the developmental processes and/or functional status of cardiac conduction system including ion channel promoter (minK-lacZ), GATA family of zinc finger proteins (GATA4), the homeodomain transcription factor (Nkx2.5), the homeodomain-only protein (Hop) and the T-box transcription factors (Tbx2, Tbx3 and Tbx5), hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) and connexins, may cause fetal arrhythmias.
|
30478614 |
2019 |
|
Heart failure
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
We generated transgenic mice (HCN4<sup>tg/wt</sup>) to assess functional consequences of HCN4 overexpression-mediated I<sub>f</sub> increase in cardiomyocytes to levels observed in human heart failure.
|
31337768 |
2019 |
|
Heart failure
|
0.040 |
Biomarker
|
disease |
BEFREE |
In this review, we summarize the current knowledge of the HCN4 channel and ivabradine, including the function of HCN4 in cardiac pacemaking, the mechanism of action of I<sub>f</sub> inhibition by ivabradine, and the pharmacological and clinical effects of ivabradine in cardiac diseases as HF, coronary artery disease, and atrial fibrillation.
|
30606942 |
2019 |
|
Congestive heart failure
|
0.040 |
Biomarker
|
disease |
BEFREE |
In this review, we summarize the current knowledge of the HCN4 channel and ivabradine, including the function of HCN4 in cardiac pacemaking, the mechanism of action of I<sub>f</sub> inhibition by ivabradine, and the pharmacological and clinical effects of ivabradine in cardiac diseases as HF, coronary artery disease, and atrial fibrillation.
|
30606942 |
2019 |
|
Congestive heart failure
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
We generated transgenic mice (HCN4<sup>tg/wt</sup>) to assess functional consequences of HCN4 overexpression-mediated I<sub>f</sub> increase in cardiomyocytes to levels observed in human heart failure.
|
31337768 |
2019 |
|
Heart Diseases
|
0.010 |
Biomarker
|
group |
BEFREE |
HCN4 is implicated in spontaneous excitation of the sinoatrial node, while channel dysfunction has been associated with sinus bradycardia, AF and structural heart disease.
|
31481236 |
2019 |
|
Hyperglycemia
|
0.010 |
Biomarker
|
disease |
BEFREE |
In streptozotocin-induced diabetic mice, ivabradine treatment significantly inhibited left ventricular hyperpolarization-activated cyclic nucleotide-gated channel 2 (HCN2) and HCN4 (major components of the I<sub>f</sub> current), activated PP2Ac, and attenuated NF-κB signaling activation and apoptosis, in line with improved histological abnormalities, fibrosis, and cardiac dysfunction without affecting hyperglycemia.
|
30998977 |
2019 |
|
Seizures
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
Specifically, seizure activity has been shown to alter the messenger RNA (mRNA) and protein expression of voltage-gated sodium channels (Na<sub>v</sub> 1.1, Na<sub>v</sub> 1.5), voltage-gated potassium channels (K<sub>v</sub> 4.2, K<sub>v</sub> 4.3), sodium-calcium exchangers (NCX1), and nonspecific cation-conducting channels (HCN2, HCN4).
|
31353444 |
2019 |
|
Tic disorder
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Together with the common KCNE1 variant S38G, previously proposed as a genetic modifier of AF, HCN4-P883R may provide a substrate for the development of AF and TIC.
|
31481236 |
2019 |
|
Generalized seizures
|
0.010 |
Biomarker
|
disease |
BEFREE |
VB-specific deletion of HCN2, but not of HCN4, also induced these generalized seizures of the absence type, corroborating a key role of HCN2 in this particular nucleus for controlling consciousness.
|
31045576 |
2019 |
|
Conduction disorder of the heart
|
0.010 |
GeneticVariation
|
group |
BEFREE |
The HCN4 gene is often present in targeted genetic testing panels for various cardiac conduction system disorders and there are several reports of HCN4 variants associated with conduction disorders.
|
30578647 |
2019 |
|
Behavioral tic
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Together with the common KCNE1 variant S38G, previously proposed as a genetic modifier of AF, HCN4-P883R may provide a substrate for the development of AF and TIC.
|
31481236 |
2019 |
|
Hyperactive behavior
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
Our data imply GSK3β activity in the protection of neuronal networks from hyper-activation in response to epileptogenic stimuli and indicate that the anti-epileptogenic function of GSK3β involves modulation of HCN4 level and the synaptic AMPA receptors pool.
|
30502054 |
2019 |
|
recurrent muscle twitches (symptom)
|
0.010 |
GeneticVariation
|
phenotype |
BEFREE |
Together with the common KCNE1 variant S38G, previously proposed as a genetic modifier of AF, HCN4-P883R may provide a substrate for the development of AF and TIC.
|
31481236 |
2019 |
|
Atrial Fibrillation
|
0.490 |
Biomarker
|
disease |
CTD_human |
Biobank-driven genomic discovery yields new insight into atrial fibrillation biology.
|
30061737 |
2018 |
|
Paroxysmal atrial fibrillation
|
0.300 |
Biomarker
|
disease |
CTD_human |
Biobank-driven genomic discovery yields new insight into atrial fibrillation biology.
|
30061737 |
2018 |
|
Persistent atrial fibrillation
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Biobank-driven genomic discovery yields new insight into atrial fibrillation biology.
|
30061737 |
2018 |
|
familial atrial fibrillation
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Biobank-driven genomic discovery yields new insight into atrial fibrillation biology.
|
30061737 |
2018 |
|
Cardiac Arrhythmia
|
0.080 |
Biomarker
|
phenotype |
BEFREE |
The transgenic overexpression of HCN4 did not induce tachycardia, but reduced heart rate variability, while the conditional knockdown of HCN4 gave rise to sinus arrhythmia.
|
29315578 |
2018 |
|
Cardiac Arrhythmia
|
0.080 |
Biomarker
|
phenotype |
BEFREE |
Unlike beta-adrenoreceptor blockade, HCN4 inhibition while lowering heart rate does not protect from atrial arrhythmias under conditions of experimental cardiac sympathetic activation.
|
29773827 |
2018 |