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Molecular Signatures of Sinus Node Dysfunction Induce Structural Remodeling in the Right Atrial Tissue

Authors
Roh, Seung-YoungKim, Ji YeonCha, Hyo KyeongLim, Hye YoungPark, YoungranLee, Kwang-NoShim, JaeminChoi, Jong-IlKim, Young-HoonSon, Gi Hoon
Issue Date
4월-2020
Publisher
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
Keywords
cardiac fibrosis; periostin; right atrium; sinus node dysfunction; transcriptome; transforming growth factor-beta
Citation
MOLECULES AND CELLS, v.43, no.4, pp.408 - 418
Indexed
SCIE
SCOPUS
KCI
Journal Title
MOLECULES AND CELLS
Volume
43
Number
4
Start Page
408
End Page
418
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/56699
DOI
10.14348/molcells.2020.2164
ISSN
1016-8478
Abstract
The sinus node (SN) is located at the apex of the cardiac conduction system, and SN dysfunction (SND)-characterized by electrical remodeling-is generally attributed to idiopathic fibrosis or ischemic injuries in the SN. SND is associated with increased risk of cardiovascular disorders, including syncope, heart failure, and atrial arrhythmias, particularly atrial fibrillation. One of the histological SND hallmarks is degenerative atrial remodeling that is associated with conduction abnormalities and increased right atrial refractoriness. Although SND is frequently accompanied by increased fibrosis in the right atrium (RA), its molecular basis still remains elusive. Therefore, we investigated whether SND can induce significant molecular changes that account for the structural remodeling of RA. Towards this, we employed a rabbit model of experimental SND, and then compared the genome-wide RNA expression profiles in RA between SND-induced rabbits and sham-operated controls to identify the differentially expressed transcripts. The accompanying gene enrichment analysis revealed extensive pro-fibrotic changes within 7 days after the SN ablation, including activation of transforming growth factor-beta (TGF-beta) signaling and alterations in the levels of extracellular matrix components and their regulators. Importantly, our findings suggest that periostin, a matricellular factor that regulates the development of cardiac tissue, might play a key role in mediating TGF-beta-signaling-induced aberrant atrial remodeling. In conclusion, the present study provides valuable information regarding the molecular signatures underlying SND-induced atrial remodeling, and indicates that periostin can be potentially used in the diagnosis of fibroproliferative cardiac dysfunctions.
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