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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005015naa a2200553 4500
001oai:DiVA.org:liu-101394
003SwePub
008131121s2013 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:127623600
024a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1013942 URI
024a https://doi.org/10.1016/j.cmet.2013.06.0032 DOI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1276236002 URI
040 a (SwePub)liud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Dong, Meiu Shandong University, Peoples R China4 aut
2451 0a Cold Exposure Promotes Atherosclerotic Plaque Growth and Instability via UCP1-Dependent Lipolysis
264 1b Elsevier (Cell Press),c 2013
338 a electronic2 rdacarrier
500 a Funding Agencies|Swedish Research Council||Swedish Cancer Foundation||Karolinska Institute Foundation||Karolinska Institute Distinguished Professor Award||Torsten Soderbergs Foundation||Tianjin Natural Science Foundation (CMM-Tianjin)|09ZCZDSF04400|ImClone Systems of Eli Lilly||European Union Integrated Project of Metoxia|222741|European Research Council (ERC) advanced grant ANGIOFAT|250021|National 973 Basic Research Program of China|2011CB5039062012CB518603|National High-Tech Research and Development Program of China|2012AA02A510|Program of Introducing Talents of Discipline to Universities|B07035|State Program of National Natural Science Foundation of China for Innovative Research Group|81021001|National Natural Science Foundation of China|811002078117325181100102812703508100012681000127|
520 a Molecular mechanisms underlying the cold-associated high cardiovascular risk remain unknown. Here, we show that the cold-triggered food-intake-independent lipolysis significantly increased plasma levels of small low-density lipoprotein (LDL) remnants, leading to accelerated development of atherosclerotic lesions in mice. In two genetic mouse knockout models (apolipoprotein E-/- [ApoE(-/-)] and LDL receptor(-/-) [Ldlr(-/-)] mice), persistent cold exposure stimulated atherosclerotic plaque growth by increasing lipid deposition. Furthermore, marked increase of inflammatory cells and plaque-associated microvessels were detected in the cold-acclimated ApoE(-/-) and Ldlr(-/-) mice, leading to plaque instability. Deletion of uncoupling protein 1 (UCP1), a key mitochondrial protein involved in thermogenesis in brown adipose tissue (BAT), in the ApoE(-/-) strain completely protected mice from the cold-induced atherosclerotic lesions. Cold acclimation markedly reduced plasma levels of adiponectin, and systemic delivery of adiponectin protected ApoE(-/-) mice from plaque development. These findings provide mechanistic insights on low-temperature-associated cardiovascular risks.
653 a MEDICINE
653 a MEDICIN
700a Yang, Xiaoyanu Shandong University, Peoples R China4 aut
700a Lim, Sharonu Karolinska Institutet4 aut
700a Cao, Ziquanu Linköpings universitet,Avdelningen för kardiovaskulär medicin,Hälsouniversitetet4 aut0 (Swepub:liu)ziqca08
700a Honek, Jenniferu Karolinska Institutet4 aut
700a Lu, Huixiau Shandong University, Peoples R China4 aut
700a Zhang, Chengu Shandong University, Peoples R China4 aut
700a Seki, Takahirou Karolinska Institutet4 aut
700a Hosaka, Kayokou Karolinska Institutet4 aut
700a Wahlberg, Ericu Östergötlands Läns Landsting,Linköpings universitet,Avdelningen för kardiovaskulär medicin,Hälsouniversitetet,Thorax-kärlkliniken i Östergötland4 aut0 (Swepub:liu)eriwa73
700a Yang, Jianminu Shandong University, Peoples R China4 aut
700a Zhang, Leiu Shandong University, Peoples R China4 aut
700a Länne, Tosteu Östergötlands Läns Landsting,Linköpings universitet,Avdelningen för kardiovaskulär medicin,Hälsouniversitetet,Thorax-kärlkliniken i Östergötland4 aut0 (Swepub:liu)tosla34
700a Sun, Baocunu Tianjin Medical University, Peoples R China4 aut
700a Li, Xuriu Sun Yat Sen University, Peoples R China4 aut
700a Liu, Yizhiu Sun Yat Sen University, Peoples R China4 aut
700a Zhang, Yunu Shandong University, Peoples R China4 aut
700a Cao, Yihaiu Karolinska Institutet4 aut
710a Karolinska Institutetb Shandong University, Peoples R China4 org
773t Cell Metabolismd : Elsevier (Cell Press)g 18:1, s. 118-129q 18:1<118-129x 1550-4131x 1932-7420
856u https://liu.diva-portal.org/smash/get/diva2:666295/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
856u http://www.cell.com/article/S1550413113002477/pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-101394
8564 8u https://doi.org/10.1016/j.cmet.2013.06.003
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:127623600

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