Heme levels are increased in human failing hearts.

ABSTRACT:

Objectives

The goal of this study was to characterize the regulation of heme and non-heme iron in human failing hearts.

Background

Iron is an essential molecule for cellular physiology, but in excess it facilitates oxidative stress. Mitochondria are the key regulators of iron homeostasis through heme and iron-sulfur cluster synthesis. Because mitochondrial function is depressed in failing hearts and iron accumulation can lead to oxidative stress, we hypothesized that iron regulation may also be impaired in heart failure (HF).

Methods

We measured mitochondrial and cytosolic heme and non-heme iron levels in failing human hearts retrieved during cardiac transplantation surgery. In addition, we examined the expression of genes regulating cellular iron homeostasis, the hem

SUBMITTER: Khechaduri A 

PROVIDER: S-EPMC3739715 | biostudies-literature | 2013 May

REPOSITORIES: biostudies-literature