Open AccessGenetic 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 Müller,
Na Li,
Xiang Wang,
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 , phospholamban , calsequestrin , ryanodine receptor , biology , genetically modified mouse , ryanodine receptor 2 , 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.