Linked Life Data

17470994

Source:http://linkedlifedata.com/resource/pubmed/id/17470994

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-5-1
pubmed:abstractText
Parathyroid gland (PTG) is a unique endocrine organ in which the quiescent glandular cells begin to proliferate in the progressive course of renal failure, leading to secondary hypereparathyroidism (SHPT). SHPT is characterized by continuous over-secretion of parathyroid hormone (PTH) and parathyroid hyperplasia, and the major contributing factors are a deficiency of active vitamin D, hypocalcemia and phosphate retention. Many experimental and human studies have revealed that the down-regulations of vitamin D receptor (VDR), calcium (Ca) -sensing receptor (CaSR), and retinoid X receptor (RXR) in parathyroid hyperplasia of SHPT, especially nodular hyperplasia, which is a severe form of hyperplasia. These also contribute to progression of parathyroid hyperplasia. Recently, mechanisms by which active vitamin D and Ca regulate parathyroid hyperplasia via their receptors have been clarified. In this paper, we review mechanisms for progression of parathyroid hyperplasia and the possibility for regression of parathyroid hyperplasia.
pubmed:language
jpn
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0917-5857
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
665-76
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
[The mechanisms of parathyroid hyperplasia and its regression].
pubmed:affiliation
Washington University School of Medicine, Department of Internal Medicine, Renal Division, USA.
pubmed:publicationType
Journal Article, English Abstract, Review