About: Role of L-type Ca2+ channels in iron transport and iron-overload cardiomyopathy

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About: Role of L-type Ca2+ channels in iron transport and iron-overload cardiomyopathy Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Role of L-type Ca2+ channels in iron transport and iron-overload cardiomyopathy
Creator	Liu, Oudit, Gavin Peter, H Backx, Maria, G Neelam, Khaper Peter, P Trivieri,
Source	PMC
abstract	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.
has issue date	2006-04-08(xsd:dateTime)
bibo:doi	10.1007/s00109-005-0029-x
bibo:pmid	16604332
has license	no-cc
sha1sum (hex)	6c5a34f395f84182f69fbf12b2533994da674185
schema:url	https://doi.org/10.1007/s00109-005-0029-x
resource representing a document's title	Role of L-type Ca2+ channels in iron transport and iron-overload cardiomyopathy
has PubMed Central identifier	PMC7095819
has PubMed identifier	16604332
schema:publication	J Mol Med (Berl)
resource representing a document's body	covid:6c5a34f395f84182f69fbf12b2533994da674185#body_text
is schema:about of	named entity 'IRON' named entity 'Iron homeostasis' named entity 'infection' named entity 'gene' named entity 'mitochondria' named entity 'Variable penetrance' named entity 'membrane lipids' named entity 'bone marrow' named entity 'ferrous' named entity 'oxidative stress' named entity 'iron overload' named entity 'excretion' named entity 'gene' named entity 'autosomal recessive inheritance pattern' named entity 'SLC11A3' named entity 'enterocytes' named entity 'Transferrin' named entity 'membrane receptor' named entity 'dilated cardiomyopathy' named entity 'LTCC' named entity 'cardiomyocytes' named entity 'untranslated regions' named entity 'myocardial contractility' named entity 'ineffective erythropoiesis' named entity 'duodenal' named entity 'imaging studies' named entity 'mRNA expression' named entity '1, 2' named entity 'oxidative stress' named entity 'intracellular' named entity 'cardiomyopathy' named entity 'iron overload' named entity 'C282Y' named entity '1, 2' named entity 'critical role' named entity 'LTCC' named entity 'parathyroid gland' named entity 'complexly' named entity 'transferrin receptor' named entity 'cardiomyopathy' named entity 'transferrin' named entity 'cytotoxicity' named entity 'macromolecular' named entity 'myocytes' named entity 'adrenocorticotrophin' named entity 'endothelial' named entity 'anemias' named entity 'iron absorption' named entity 'cardiomyocytes' named entity 'IREs' named entity 'beta-globulin' named entity 'hemochromatosis' named entity 'Type 1' named entity 'sarcoplasmic reticulum' named entity 'pathophysiological' named entity 'iron metabolism' named entity 'HFE2' named entity 'anti-oxidative' named entity 'uncorrelated' named entity 'bradycardia' named entity 'histological' named entity 'puberty' named entity 'excitable tissues' named entity 'pancreatic beta cells' named entity 'LTCC' named entity 'ferrous' named entity 'ferroportin' named entity 'red blood cells' named entity 'intestine' named entity 'redox cycling' named entity 'LTCC' named entity 'iron overload' named entity 'verapamil' named entity 'cytoplasmic'

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