Trpm4 gene invalidation leads to cardiac hypertrophy and electrophysiological alterations.

ABSTRACT:

Rationale

TRPM4 is a non-selective Ca2+-activated cation channel expressed in the heart, particularly in the atria or conduction tissue. Mutations in the Trpm4 gene were recently associated with several human conduction disorders such as Brugada syndrome. TRPM4 channel has also been implicated at the ventricular level, in inotropism or in arrhythmia genesis due to stresses such as ß-adrenergic stimulation, ischemia-reperfusion, and hypoxia re-oxygenation. However, the physiological role of the TRPM4 channel in the healthy heart remains unclear.

Objectives

We aimed to investigate the role of the TRPM4 channel on whole cardiac function with a Trpm4 gene knock-out mouse (Trpm4-/-) model.

Methods and results

Morpho-functional analysis revealed left ventricular (LV) eccent

SUBMITTER: Demion M 

PROVIDER: S-EPMC4274076 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature