Gap junction remodelling in human heart failure is associated with increased interaction of connexin43 with ZO-1.

ABSTRACT:

Aims

Remodelling of gap junctions, involving reduction of total gap junction quantity and down-regulation of connexin43 (Cx43), contributes to the arrhythmic substrate in congestive heart failure. However, little is known of the underlying mechanisms. Recent studies from in vitro systems suggest that the connexin-interacting protein zonula occludens-1 (ZO-1) is a potential mediator of gap junction remodelling. We therefore examined the hypothesis that ZO-1 contributes to reduced expression of Cx43 gap junctions in congestive heart failure.

Methods and results

Left ventricular myocardium from healthy control human hearts (n = 5) was compared with that of explanted hearts from transplant patients with end-stage congestive heart failure due to idiopathic dilated cardiomyopathy

SUBMITTER: Bruce AF 

PROVIDER: S-EPMC5436744 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature