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Sökning: WFRF:(Stenvinkel Peter) > Alkaline phosphatas...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003697naa a2200385 4500
001oai:DiVA.org:liu-138880
003SwePub
008170627s2017 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:136002052
024a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1388802 URI
024a https://doi.org/10.1038/nrneph.2017.602 DOI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1360020522 URI
040 a (SwePub)liud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a for2 swepub-publicationtype
100a Haarhaus, Mathiasu Karolinska Institutet,Linköpings universitet,Institutionen för klinisk och experimentell medicin,Medicinska fakulteten,Region Östergötland, Klinisk kemi,Karolinska Institute, Sweden4 aut0 (Swepub:liu)matha60
2451 0a Alkaline phosphatase: a novel treatment target for cardiovascular disease in CKD
264 c 2017-05-15
264 1b NATURE PUBLISHING GROUP,c 2017
338 a print2 rdacarrier
520 a Cardiovascular disease is the main cause of early death in the settings of chronic kidney disease (CKD), type 2 diabetes mellitus (T2DM), and ageing. Cardiovascular events can be caused by an imbalance between promoters and inhibitors of mineralization, which leads to vascular calcification. This process is akin to skeletal mineralization, which is carefully regulated and in which isozymes of alkaline phosphatase (ALP) have a crucial role. Four genes encode ALP isozymes in humans. Intestinal, placental and germ cell ALPs are tissue-specific, whereas the tissue-nonspecific isozyme of ALP (TNALP) is present in several tissues, including bone, liver and kidney. TNALP has a pivotal role in bone calcification. Experimental overexpression of TNALP in the vasculature is sufficient to induce vascular calcification, cardiac hypertrophy and premature death, mimicking the cardiovascular phenotype often found in CKD and T2DM. Intestinal ALP contributes to the gut mucosal defence and intestinal and liver ALPs might contribute to the acute inflammatory response to endogenous or pathogenic stimuli. Here we review novel mechanisms that link ALP to vascular calcification, inflammation, and endothelial dysfunction in kidney and cardiovascular diseases. We also discuss new drugs that target ALP, which have the potential to improve cardiovascular outcomes without inhibiting skeletal mineralization.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng
700a Brandenburg, Vincentu RWTH University Hospital Aachen, Germany4 aut
700a Kalantar-Zadeh, Kamyaru University of Calif Irvine, CA 92868 USA; University of Calif Los Angeles, CA 90502 USA4 aut
700a Stenvinkel, Peteru Karolinska Institutet,Karolinska Institute, Sweden4 aut
700a Magnusson, Peru Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten,Region Östergötland, Klinisk kemi4 aut0 (Swepub:liu)perma28
710a Linköpings universitetb Institutionen för klinisk och experimentell medicin4 org
773t Nature Reviews Nephrologyd : NATURE PUBLISHING GROUPg 13:7, s. 429-442q 13:7<429-442x 1759-5061x 1759-507X
856u https://escholarship.org/content/qt6xf830zr/qt6xf830zr.pdf?t=q06sqx
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-138880
8564 8u https://doi.org/10.1038/nrneph.2017.60
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:136002052

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