Linked Life Data

18282520

Source:http://linkedlifedata.com/resource/pubmed/id/18282520

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-2-19
pubmed:abstractText
Erythrocytes require iron to perform their duty as oxygen carriers. Mammals have evolved a mechanism to maintain systemic iron within an optimal range that fosters erythroid development and function while satisfying other body iron needs. This chapter reviews erythroid iron uptake and utilization as well as systemic factors that influence iron availability. One of these factors is hepcidin, a circulating peptide hormone that maintains iron homeostasis. Elevated levels of hepcidin in the bloodstream effectively shut off iron absorption by disabling the iron exporter ferroportin. Conversely, low levels of circulating hepcidin allow ferroportin to export iron into the bloodstream. Aberrations in hepcidin expression or responsiveness to hepcidin result in disorders of iron deficiency and iron overload. It is clear that erythroid precursors communicate their iron needs to the liver to influence the production of hepcidin and thus the amount of iron available for use. However, the mechanism by which erythroid cells accomplish this remains unclear and is an area of active investigation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0070-2153
pubmed:author
pubmed:issnType
Print
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
141-67
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Iron homeostasis and erythropoiesis.
pubmed:affiliation
Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
pubmed:publicationType
Journal Article, Review