Cold exposure promotes atherosclerotic plaque growth and instability via UCP1-dependent lipolysis
Dong M, Yang X, Lim S, Cao Z, Honek J, Lu H, Zhang C, Seki T, Hosaka K, Wahlberg E, Yang J, Zhang L, Länne T, Sun B, Li X, Liu Y, Zhang Y, Cao Y
Cell metabolism · 184 citations
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- Animals
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
- Government
- European Research Council
Based on 1 listed funder(s).
Publication
- Published
- 2013-07-01 · Cell Metab · vol. 18 · issue 1 · pp. 118–129
- Publisher
- Cell Press
- Cited
- 244 citations · more than 99% of similar papers · 10.5× the field average
- Impact
- Top 10% most cited in its field
- References
- 39 works
- Access
- Open access (hybrid journal) · CC-BY
- Research areas
- Adipose Tissue and Metabolism · Cardiovascular Disease and Adiposity · Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- Apolipoprotein E, LDL receptor, Endocrinology, Internal medicine, Adiponectin, Lipolysis, Knockout mouse, Receptor, Biology, Thermogenesis, Lipoprotein, Adipose tissue, Medicine, Cholesterol, Diabetes mellitus, Insulin resistance
- MeSH
- animals, mice, knockout, humans, mice, disease models, animal, apolipoproteins e, ion channels, receptors, ldl, mitochondrial proteins, pilot projects, acclimatization, lipolysis, thermogenesis, adult, middle aged, female, male, atherosclerosis, lipid metabolism, adiponectin, cholesterol, ldl, adipose tissue, brown, cold temperature, plaque, atherosclerotic, uncoupling protein 1
18 authors
From SE, CN
- Mei DongKarolinska Institutet; Qilu Hospital of Shandong University
- Xiaoyan YangKarolinska Institutet; Qilu Hospital of Shandong University
- Sharon LimKarolinska Institutet
- Ziquan CaoLinköping University
- Jennifer HonekKarolinska Institutet
- Huixia LuQilu Hospital of Shandong University
Abstract
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.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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