Results 81 to 90 of about 6,848 (166)

Bioprinted Excitable Tissues with Multistimulation Systems for Promoting Function and Maturation

Advanced NanoBiomed Research, Volume 6, Issue 3, March 2026.
This review provides an overview of stimulation strategies used to enhance the functional maturation of bioprinted excitable tissues. It addresses key limitations in physiological performance of bioprinted excitable tissues, outlines major stimulation modalities—including electrical, mechanical, optical, magnetic, ultrasound, and hybrid—and examines ...
Uijung Yong, Jinseon Park, Jinah Jang
wiley   +1 more source

In vivo KCNH2-suppression-replacement gene therapy attenuates the pathogenic phenotype in transgenic rabbits with short QT syndrome type 1

Europace
Background Short QT syndrome type 1 (SQT1) is a genetic channelopathy characterized by gain-of-function variants in the KCNH2-encoded potassium channel underlying the IKr current, leading to a pathologically shortened cardiac action potential duration ...
S. Nimani, S. Bains, N. Alerni, L. Giammarino, J. Louradour, A. Horváth, O. Beslac, D. Tester, N. Christoforou, M. Brunner, D. Casoni, A. Haeberlin, G. Brooks, M. J. Ackerman, K. Odening   +14 more
semanticscholar   +1 more source

Cardiac Manifestations of KCNK17 Mutations and/or Polymorphisms: A Systematic Review

Health Science Reports, Volume 9, Issue 3, March 2026.
ABSTRACT Background and Aims The KCNK17 gene encodes k2p17.1 channels (TASK‐4 or TALK‐2) with dominant expressions in the atria and the Purkinje fibers. Emerging studies have suggested possible associations between KCNK17 variants and cardiovascular as well as cerebrovascular diseases. This review aimed to systematically evaluate the evidence on KCNK17
Amir Askarinejad, Mahshid Malakootian, Dorsa Shekouh, Amirreza Sabahizadeh, Majid Haghjoo   +4 more
wiley   +1 more source

Long QT Syndrome Type 2: Emerging Strategies for Correcting Class 2 KCNH2 (hERG) Mutations and Identifying New Patients

Biomolecules, 2020
Significant advances in our understanding of the molecular mechanisms that cause congenital long QT syndrome (LQTS) have been made. A wide variety of experimental approaches, including heterologous expression of mutant ion channel proteins and the use of
Makoto Ono, Don E. Burgess, Elizabeth A. Schroder, Claude S. Elayi, Corey L. Anderson, Craig T. January, Bin Sun, Kalyan Immadisetty, Peter M. Kekenes-Huskey, Brian P. Delisle   +9 more
doaj   +1 more source

Quantitative Histological Insights Into Sudden Arrhythmic Death Syndrome: Findings From a Forensic Autopsy Cohort

APMIS, Volume 134, Issue 3, March 2026.
ABSTRACT Sudden arrhythmic death syndrome (SADS) is a major cause of sudden cardiac death in young individuals, characterized by structurally normal hearts and negative toxicology. Although guidelines recommend family screening, phenotyping remains challenging.
Pernille Heimdal Holm, Thomas Hartvig Lindkær Jensen, Joseph Westaby, Mary Sheppard, Stine Bøttcher Jacobsen, Mikkel Eriksen Dupont, Jeppe Dyrberg Andersen, Bo Gregers Winkel, Jacob Tfelt‐Hansen, Jytte Banner, Kristine Boisen Olsen   +10 more
wiley   +1 more source

A Rare Case of the Digenic Inheritance of Long QT Syndrome Type 2 and Type 6

Case Reports in Medicine, 2019
We report a 37-year-old woman with an out-of-hospital cardiac arrest caused by ventricular fibrillation due to digenic inheritance of long QT syndrome type 2 (KCNH2 gene) and type 6 (KCNE2 gene).
Annejet Heida, Lisette J. M. E. van der Does, Ahmed A. Y. Ragab, Natasja M. S. de Groot   +3 more
doaj   +1 more source

Generation and characterization of an induced pluripotent stem cell (iPSC) line (NUIGi003-A) from a long QT syndrome type 2 (LQT2) patient harbouring the KCNH2 c.2464G>A pathogenic variant

Stem Cell Research, 2020
Long QT syndrome (LQTS), an inherited cardiac ion channelopathy, is associated with ventricular arrhythmias and risk of sudden death. LQTS sub-type 2 (LQT2) is caused by pathogenic variants in KCNH2 encoding the α-subunit of Kv11.1, thus affecting the ...
Ning Ge, Min Liu, Janusz Krawczyk, Veronica McInerney, Deirdre Ward, Sanbing Shen, Timothy O'Brien, Terence Prendiville   +7 more
doaj   +1 more source

Mutual Exclusion Analysis Shows that DUSP9 Negatively Regulates PD‐L1 Expression and Acts as a Target to Enhance Anti‐PD‐1 Efficacy

Advanced Science, Volume 13, Issue 12, 27 February 2026.
A mutually exclusive screening system is established to identify negative regulators of highly plastic genes. Dual specificity phosphatase (DUSP9) is a novel negative regulatory molecule of PD‐L1 by dephosphorylating STAT3, and acts as a target molecule in combination with PD‐1 antibody for tumor immunotherapy and a new clinical biomarker for ...
Yuzhe Hu, Ling Tang, Zheng Kuang, Danyi Huang, Ting Li, Gaofei Yin, Yingyu Chen, Wei Guo, Wenling Han, Pingzhang Wang   +9 more
wiley   +1 more source

AI-driven network pharmacology and multi-omics validation identify KCNH2 as a prognostic biomarker and candidate therapeutic vulnerability of Acorus tatarinowii in glioblastoma

Frontiers in Pharmacology
BackgroundGlioblastoma (GBM) remains a highly aggressive malignancy with limited effective therapeutic options. Integrating traditional medicine resources with artificial intelligence–based analytical strategies may accelerate the identification of novel
Xiaoqing Song, Yuanyang Xiao, Junhui Liu, Shanshan Wei, Meijuan Tan, Yuanyuan Chen, Xiaohong Yu   +6 more
doaj   +1 more source

Identification and characterization of two novel KCNH2 mutations contributing to long QT syndrome.

PLoS ONE
We identified two different inherited mutations in KCNH2 gene, or human ether-a-go-go related gene (hERG), which are linked to Long QT Syndrome. The first mutation was in a 1-day-old infant, whereas the second was in a 14-year-old girl.
Anthony Owusu-Mensah, Jacqueline Treat, Joyce Bernardi, Ryan Pfeiffer, Robert Goodrow, Bright Tsevi, Victoria Lam, Michel Audette, Jonathan M Cordeiro, Makarand Deo   +9 more
doaj   +1 more source