The involvement of ZnT-1, a new modulator of cardiac L-type calcium channels, in [corrected] atrial tachycardia remodeling. [corrected].
Ann N Y Acad Sci
; 1188: 87-95, 2010 Feb.
Article
em En
| MEDLINE
| ID: mdl-20201890
ABSTRACT
Atrial fibrillation (AF), the highest occurring cardiac arrhythmia in the Western world, is associated with substantial morbidity and increased mortality. In spite of extensive research, the cause of atrial electrical remodeling, a major factor in the self-perpetuating nature of AF, is still unknown. Downregulation of L-type Ca2+ channel (LTCC) activity is the hallmark of atrial electrical remodeling. ZnT-1 is a ubiquitous membrane protein that was recently suggested to inhibit the LTCC. We have studied and shown that ZnT-1 expression inhibits LTCC function in an oocyte expression system as well as in isolated cardiomyocytes. Our data also show that rapid electrical pacing can augment ZnT-1 expression in culture as well as in the atria of rats in vivo. Finally, in a pilot study, ZnT-1 expression was found to be augmented in the atria of AF patients. These findings position ZnT-1 as a probable missing link in the mechanism underlying atrial tachycardia remodeling.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Taquicardia
/
Doença da Artéria Coronariana
/
Canais de Cálcio Tipo L
/
Proteínas de Xenopus
/
Proteínas de Transporte de Cátions
/
Proteínas de Membrana
Limite:
Animals
/
Humans
/
Male
Idioma:
En
Revista:
Ann N Y Acad Sci
Ano de publicação:
2010
Tipo de documento:
Article
País de afiliação:
Israel