Show simple item record

dc.contributor.authorBai, Jieyun; email: baijieyun@jnu.edu.cn
dc.contributor.authorLu, Yaosheng; email: tluys@jnu.edu.cn
dc.contributor.authorZhu, Yijie; email: zyj1934261010@stu2019.jnu.edu.cn
dc.contributor.authorWang, Huijin; email: twanghj@jnu.edu.cn
dc.contributor.authorYin, Dechun; email: yindechun0429@163.com
dc.contributor.authorZhang, Henggui; email: henggui.zhang@manchester.ac.uk
dc.contributor.authorFranco, Diego; orcid: 0000-0002-5669-7164; email: dfranco@ujaen.es
dc.contributor.authorZhao, Jichao; email: j.zhao@auckland.ac.nz
dc.date.accessioned2021-07-23T16:16:05Z
dc.date.available2021-07-23T16:16:05Z
dc.date.issued2021-07-19
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625338/ijms-22-07681.xml?sequence=2
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625338/additional-files.zip?sequence=3
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625338/ijms-22-07681.pdf?sequence=4
dc.identifier.citationInternational Journal of Molecular Sciences, volume 22, issue 14, page e7681
dc.identifier.urihttp://hdl.handle.net/10034/625338
dc.descriptionFrom MDPI via Jisc Publications Router
dc.descriptionHistory: accepted 2021-07-16, pub-electronic 2021-07-19
dc.descriptionPublication status: Published
dc.descriptionFunder: National Key Research and Development Program of China; Grant(s): 2019YFC0120100, 2019YFC0121907
dc.descriptionFunder: National Natural Science Foundation of China; Grant(s): 61901192
dc.description.abstractAtrial fibrillation (AF) is a common arrhythmia. Better prevention and treatment of AF are needed to reduce AF-associated morbidity and mortality. Several major mechanisms cause AF in patients, including genetic predispositions to AF development. Genome-wide association studies have identified a number of genetic variants in association with AF populations, with the strongest hits clustering on chromosome 4q25, close to the gene for the homeobox transcription PITX2. Because of the inherent complexity of the human heart, experimental and basic research is insufficient for understanding the functional impacts of PITX2 variants on AF. Linking PITX2 properties to ion channels, cells, tissues, atriums and the whole heart, computational models provide a supplementary tool for achieving a quantitative understanding of the functional role of PITX2 in remodelling atrial structure and function to predispose to AF. It is hoped that computational approaches incorporating all we know about PITX2-related structural and electrical remodelling would provide better understanding into its proarrhythmic effects leading to development of improved anti-AF therapies. In the present review, we discuss advances in atrial modelling and focus on the mechanistic links between PITX2 and AF. Challenges in applying models for improving patient health are described, as well as a summary of future perspectives.
dc.languageen
dc.publisherMDPI
dc.rightsLicence for this article: https://creativecommons.org/licenses/by/4.0/
dc.sourceeissn: 1422-0067
dc.subjectcardiac arrhythmias
dc.subjectatrial fibrillation
dc.subjectPITX2
dc.subjectcomputational model
dc.subjectelectrical remodelling
dc.subjectstructural remodelling
dc.subjectcalcium handling
dc.subjectmRNA
dc.subjectelectrophysiology
dc.titleUnderstanding PITX2-Dependent Atrial Fibrillation Mechanisms through Computational Models
dc.typearticle
dc.date.updated2021-07-23T16:16:05Z
dc.date.accepted2021-07-16


Files in this item

Thumbnail
Name:
ijms-22-07681.xml
Size:
10.07Kb
Format:
XML
Thumbnail
Name:
additional-files.zip
Size:
903.7Kb
Format:
Unknown
Thumbnail
Name:
ijms-22-07681.pdf
Size:
5.076Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record