Erratum to: Transcriptome and proteome mapping in the sheep atria reveal molecular features of atrial fibrillation progression

Alvarez-Franco, Alba; Rouco, Raquel; Ramírez, Rafael J.; Guerrero-Serna, Guadalupe; Tiana, María; Cogliati, Sara; Kaur, Kuljeet; Saeed, M. A.; Magni, Ricardo; Enrı́quez, José Antonio; Sánchez-Cabo, Fátima; Jalife, José; Manzanares, Miguel

doi:10.1093/cvr/cvab216

Cited by 1 publication

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“…This is not observed in the AF group (lacking AVB), which may indicate that this adaptation has already occurred. This idea would be consistent with the downregulation of chromatin-related genes recently noted in the atria of sheep AF models 36 and may be a result of earlier establishment of profibrotic transdifferentiation in AF compared with AF+AVB canine models.…”

Section: Discussionsupporting

confidence: 86%

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Transcriptomic Profiling of Canine Atrial Fibrillation Models After One Week of Sustained Arrhythmia

Leblanc

Hassani

Liesinger

et al. 2021

Circ: Arrhythmia and Electrophysiology

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Background - Atrial fibrillation (AF), the most common sustained arrhythmia, is associated with increased morbidity, mortality, and health-care costs. AF develops over many years and is often related to substantial atrial structural and electrophysiological remodeling. AF may lack symptoms at onset and atrial biopsy samples are generally obtained in subjects with advanced disease, so it is difficult to study earlier-stage pathophysiology in humans. Methods - Here, we characterized comprehensively the transcriptomic (miRNAseq and mRNAseq) changes in the left atria of two robust canine AF-models after one week of electrically-maintained AF, without or with ventricular rate-control via atrioventricular node-ablation/ventricular pacing. Results - Our RNA-sequencing experiments identified thousands of genes that are differentially expressed, including a majority that have never before been implicated in AF. Gene-set enrichment analyses highlighted known (e.g. extracellular matrix structure organization) but also many novel pathways (e.g. muscle structure development, striated muscle cell differentiation) that may play a role in tissue remodeling and/or cellular trans-differentiation. Of interest, we found dysregulation of a cluster of non-coding RNAs, including many microRNAs but also the MEG3 long non-coding RNA orthologue, located in the syntenic region of the imprinted human DLK1-DIO3 locus. Interestingly (in the light of other recent observations), our analysis identified gene-targets of differentially expressed microRNAs at the DLK1-DIO3 locus implicating glutamate signaling in AF pathophysiology. Conclusions - Our results capture molecular events that occur at an early stage of disease development using well-characterized animal models, and may therefore inform future studies that aim to further dissect the causes of AF in humans.

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Section: Discussionsupporting

confidence: 86%

“…This finding is concordant with the many chromatin remodeling genes dysregulated in our models, which is an emerging phenotype of AF both in human and sheep models. 36 Molecular Remodeling in AF With Versus Without AVB…”

Section: Discussionmentioning

confidence: 99%