Results 41 to 50 of about 313 (129)

Caenorhabditis elegans as an in vivo model system for human inherited primary arrhythmia syndromes

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Most genes involved in inherited primary arrhythmia syndromes (IPAS) are conserved in Caenorhabditis elegans, where genetic manipulation enables functional characterization of variants, identification of regulatory proteins, and in vivo drug testing.
Antoine Delinière   +6 more
wiley   +1 more source

Hydroxymethylation of microRNA-365-3p Regulates Nociceptive Behaviors via Kcnh2 [PDF]

open access: yesThe Journal of Neuroscience, 2016
DNA 5-hydroxylmethylcytosine (5hmC) catalyzed by ten-eleven translocation methylcytosine dioxygenase (TET) occurs abundantly in neurons of mammals. However, thein vivocausal link between TET dysregulation and nociceptive modulation has not been established.
Zhiqiang, Pan   +9 more
openaire   +2 more sources

Translating cardiovascular ion channel and Ca2+ signalling mechanisms into therapeutic insights

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend This white paper integrates mechanistic discoveries across ion channel biology, Ca2+ signalling and multiscale cardiovascular physiology to highlight new opportunities for accelerating research and guiding next‐generation therapies. Printed with permission from ®Anita Impagliazzo Medical Illustration. [Correction added on 2 March
Silvia Marchianò   +18 more
wiley   +1 more source

Age‐ and sex‐specific modulation of human cardiac electrophysiology by doxorubicin

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend DOX differentially impacts cardiac electrophysiology based on sex and age. Sex differences were primarily observed among younger hearts, where action potential duration (APD) prolongation was observed in females, but not in males. Created using BioRender. George, S. (2026) https://BioRender.com/wresf1k Abstract Acute doxorubicin (
Sharon A. George   +5 more
wiley   +1 more source

Potassium voltage-gated channel subfamily H member 2 (KCNH2) is a promising target for incretin secretagogue therapies

open access: yesSignal Transduction and Targeted Therapy
Derived from enteroendocrine cells (EECs), glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are pivotal incretin hormones crucial for blood glucose regulation.
Ying-Chao Yuan   +6 more
doaj   +1 more source

Voltage‐gated potassium channels mediate thyroid hormone control of skeletal muscle excitability

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Thyroid hormone (TH)‐dependent remodelling of potassium (K+) channel networks regulates skeletal muscle (SkM) excitability. Triiodothyronine (T3), locally generated from thyroxine (T4) by type 2 deiodinase (D2), binds thyroid hormone receptors (TRα/β) and modulates transcription via thyroid response elements (TREs).
Annarita Nappi   +12 more
wiley   +1 more source

Case Report: Biventricular Noncompaction Cardiomyopathy With Pulmonary Stenosis and Bradycardia in a Fetus With KCNH2 Mutation

open access: yesFrontiers in Genetics, 2022
Background: Left ventricular noncompaction (LVNC) is a rare cardiomyopathy, long QT syndrome (LQTS) is a rare ion channel disease, and simultaneous occurrence of both is even rarer.
Hairui Sun   +8 more
doaj   +1 more source

hERG1 channels and potential therapeutics for long QT syndrome

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Prolonged QT results from hERG1 channel dysfunction. (A) Physiological anterograde trafficking of hERG1 channels to the plasma membrane, leading to a normal electrocardiogram. (B) Prolonged QT results from the presence of fewer hERG1 channels on the plasma membrane due to decreased anterograde trafficking or reduced function due ...
Elizabeth H. Schneider   +3 more
wiley   +1 more source

Silencing the Mutant KCNH2 Allele to Reduce the Effects of Long QT Syndrome Type 2

open access: yesFrontiers in Bioscience-Landmark
Background: Long-QT syndrome type 2 (LQTS2), which is associated with life-threatening cardiac arrhythmias, is caused by pathogenic heterozygous loss-of-function mutations in the KCNH2 gene.
Ronald Wilders
doaj   +1 more source

Optimization of novel compounds using computer‐aided drug design for treatment of cardiac arrhythmia

open access: yesBritish Journal of Pharmacology, Volume 183, Issue 17, Page 5407-5420, September 2026.
Background and Purpose Loss‐of‐function mutations of the voltage‐gated Kv7.1 (KCNQ/KCNE1) channels lead to cardiac arrhythmia such as long QT syndrome, characterized by a prolonged QT interval . One strategy to correct the prolonged QT interval is to design molecules that activate KCNQ1/KCNE1 channels and restore the QT interval.
Jessica Jowais   +4 more
wiley   +1 more source

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