The involvement of ZnT-1, a new modulator of cardiac L-type calcium channels, in remodeling atrial tachycardia

Ofer Beharier, Yoram Etzion, Shiri Levi, Merav Mor, Michal Mor, Shani Dror, Joy Kahn, Amos Katz, Arie Moran

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

6 Scopus citations

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.

Original languageEnglish
Title of host publicationAnalysis of Cardiac Development
Subtitle of host publicationFrom Embryo to Old Age
PublisherBlackwell Publishing Inc.
Pages87-95
Number of pages9
ISBN (Print)9781573317474
DOIs
StatePublished - 1 Jan 2010

Publication series

NameAnnals of the New York Academy of Sciences
Volume1188
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Atrial electrical remodeling
  • Atrial fibrillation
  • Cation diffusion facilitator proteins
  • L-type calcium channels
  • Rapid pacing
  • ZnT-1

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