Role of L-type Ca2+ channels in iron transport and iron-overload
cardiomyopathy.
Oudit GY, Trivieri MG, Khaper N, Liu PP, Backx PH
J Mol Med. 2006 Apr 8;

Excessive body iron or iron overload occurs under conditions such as
primary (hereditary) hemochromatosis and secondary iron overload
(hemosiderosis), which are reaching epidemic levels worldwide. Primary
hemochromatosis is the most common genetic disorder with an allele
frequency greater than 10% in individuals of European ancestry, while
hemosiderosis is less common but associated with a much higher
morbidity and mortality. Iron overload leads to iron deposition in many
tissues especially the liver, brain, heart and endocrine tissues.
Elevated cardiac iron leads to diastolic dysfunction, arrhythmias and
dilated cardiomyopathy, and is the primary determinant of survival in
patients with secondary iron overload as well as a leading cause of
morbidity and mortality in primary hemochromatosis patients. In
addition, iron-induced cardiac injury plays a role in acute iron
toxicosis (iron poisoning), myocardial ischemia-reperfusion injury,
Friedreich ataxia and neurodegenerative diseases. Patients with iron
overload also routinely suffer from a range of endocrinopathies,
including diabetes mellitus and anterior pituitary dysfunction. Despite
clear connections between elevated iron and clinical disease, iron
transport remains poorly understood. While low-capacity divalent metal
and transferrin-bound transporters are critical under normal
physiological conditions, L-type Ca(2+) channels (LTCC) are
high-capacity pathways of ferrous iron (Fe(2+)) uptake into
cardiomyocytes especially under iron overload conditions. Fe(2+) uptake
through L-type Ca(2+) channels may also be crucial in other excitable
cells such as pancreatic beta cells, anterior pituitary cells and
neurons. Consequently, LTCC blockers represent a potential new therapy
to reduce the toxic effects of excess iron.

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