Stretch-activated two-pore-domain (K2P) potassium channels in the heart: Focus on atrial fibrillation and heart failure.
作者： Constanze Schmidt , Felix Wiedmann , Stefan M. Kallenberger , Antonius Ratte , Jan S. Schulte
DOI: 10.1016/J.PBIOMOLBIO.2017.05.004
关键词: Heart failure 、 Potassium channel 、 Transgene 、 Chemistry 、 Atrial fibrillation 、 Heart disease 、 Mechanosensitive channels 、 Downregulation and upregulation 、 Messenger RNA 、 Endocrinology 、 Internal medicine
摘要: Abstract Two-pore-domain potassium (K 2P ) channels modulate cellular excitability. The significance of stretch-activated cardiac K 2.1, TREK-1, KCNK 2; 4.1, TRAAK, 4; 10.1, TREK-2, 10) in heart disease has not been elucidated detail. aim this work was to assess expression and remodeling mechanosensitive atrial fibrillation (AF) failure (HF) patients comparison murine models. Cardiac channel levels were quantified (A) ventricular (V) tissue obtained from undergoing open surgery. In addition, control mice mouse models AF (cAMP-response element modulator (CREM)-IbΔC-X transgenic animals) or HF (cardiac dysfunction induced by transverse aortic constriction, TAC) employed. Human 2 displayed highest mRNA abundance among members the family (V > A). Disease-associated 2.1 studied with impaired left function, 2.1) protein significantly reduced. subjects, downregulation observed. AF-associated suppression Kcnk recapitulated CREM-transgenic mice. Ventricular altered disease. conclusion, 10.1 + are expressed throughout heart. HF- suggest a mechanistic contribution arrhythmogenesis.
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