期刊
CELL METABOLISM
卷 18, 期 1, 页码 118-129出版社
CELL PRESS
DOI: 10.1016/j.cmet.2013.06.003
关键词
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资金
- 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 [2011CB503906, 2012CB518603]
- 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 [81100207, 81173251, 81100102, 81270350, 81000126, 81000127]
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.
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