Hyperactive ryanodine receptors in human heart failure and ischaemic cardiomyopathy reside outside of couplons.

ABSTRACT:

Aims

In ventricular myocytes from humans and large mammals, the transverse and axial tubular system (TATS) network is less extensive than in rodents with consequently a greater proportion of ryanodine receptors (RyRs) not coupled to this membrane system. TATS remodelling in heart failure (HF) and after myocardial infarction (MI) increases the fraction of non-coupled RyRs. Here we investigate whether this remodelling alters the activity of coupled and non-coupled RyR sub-populations through changes in local signalling. We study myocytes from patients with end-stage HF, compared with non-failing (non-HF), and myocytes from pigs with MI and reduced left ventricular (LV) function, compared with sham intervention (SHAM).

Methods and results

Single LV myocytes for functional studi

SUBMITTER: Dries E 

PROVIDER: S-EPMC6106102 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature