Genetic inhibition of nuclear factor of activated T-cell c2 prevents atrial fibrillation in CREM transgenic mice | Zendy

Li Ni | Zendy; Satadru K. Lahiri | Zendy; Jiali Nie | Zendy; Xiaolu Pan | Zendy; Issam Abu-Taha | Zendy; Julia O. Reynolds | Zendy; Hannah M. Campbell | Zendy; Haihao Wang | Zendy; Markus Kamler | Zendy; Wilhelm Schmitz | Zendy; Frank U. Müller | Zendy; Na Li | Zendy; Wei Xiang | Zendy; Dao Wen Wang | Zendy; Dobromir Dobrev | Zendy; Xander H.T. Wehrens | Zendy

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Genetic inhibition of nuclear factor of activated T-cell c2 prevents atrial fibrillation in CREM transgenic mice

Author(s) -

Li Ni,

Satadru K. Lahiri,

Jiali Nie,

Xiaolu Pan,

Issam Abu-Taha,

Julia O. Reynolds,

Hannah M. Campbell,

Haihao Wang,

Markus Kamler,

Wilhelm Schmitz,

Frank U. Müller,

Na Li,

Wei Xiang,

Dao Wen Wang,

Dobromir Dobrev,

Xander H.T. Wehrens

Publication year - 2021

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvab325

Subject(s) - nfat , medicine , endocrinology , ryanodine receptor , phospholamban , calsequestrin , ryanodine receptor 2 , genetically modified mouse , biology , knockout mouse , transgene , receptor , calcineurin , heart failure , biochemistry , transplantation , gene

Abnormal intracellular calcium (Ca2+) handling contributes to the progressive nature of atrial fibrillation (AF), the most common sustained cardiac arrhythmia. Evidence in mouse models suggests that activation of the nuclear factor of activated T-cell (NFAT) signalling pathway contributes to atrial remodelling. Our aim was to determine the role of NFATc2 in AF in humans and mouse models.

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