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Targeting the Brain to Protect the Heart.

作者信息

Lopaschuk Gary D

机构信息

Cardiovascular Research Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.

出版信息

JACC Basic Transl Sci. 2021 Jan 25;6(1):71-73. doi: 10.1016/j.jacbts.2020.12.004. eCollection 2021 Jan.

DOI:10.1016/j.jacbts.2020.12.004
PMID:33533757
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7838095/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf4/7838095/42f228bc86e0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf4/7838095/4a0c8391ac9b/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf4/7838095/42f228bc86e0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf4/7838095/4a0c8391ac9b/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf4/7838095/42f228bc86e0/gr1.jpg

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本文引用的文献

1
Restoration of Cardiac Function After Myocardial Infarction by Long-Term Activation of the CNS Leptin-Melanocortin System.通过长期激活中枢神经系统瘦素-黑皮质素系统恢复心肌梗死后的心功能
JACC Basic Transl Sci. 2021 Jan 25;6(1):55-70. doi: 10.1016/j.jacbts.2020.11.007. eCollection 2021 Jan.
2
Weight loss enhances cardiac energy metabolism and function in heart failure associated with obesity.体重减轻可增强肥胖相关性心力衰竭患者的心脏能量代谢和功能。
Diabetes Obes Metab. 2019 Aug;21(8):1944-1955. doi: 10.1111/dom.13762. Epub 2019 Jun 4.
3
Failing mouse hearts utilize energy inefficiently and benefit from improved coupling of glycolysis and glucose oxidation.
衰竭的老鼠心脏能量利用效率低下，受益于糖酵解和葡萄糖氧化偶联的改善。
Cardiovasc Res. 2014 Jan 1;101(1):30-8. doi: 10.1093/cvr/cvt216. Epub 2013 Sep 17.
4
Leptin signalling reduces the severity of cardiac dysfunction and remodelling after chronic ischaemic injury.瘦素信号传导可减轻慢性缺血性损伤后心脏功能障碍和重塑的严重程度。
Cardiovasc Res. 2008 Jan;77(1):54-63. doi: 10.1093/cvr/cvm023. Epub 2007 Sep 20.
5
Epinephrine increases ATP production in hearts by preferentially increasing glucose metabolism.肾上腺素通过优先增加葡萄糖代谢来提高心脏中的ATP生成。
Am J Physiol. 1994 Nov;267(5 Pt 2):H1862-71. doi: 10.1152/ajpheart.1994.267.5.H1862.
6
High rates of fatty acid oxidation during reperfusion of ischemic hearts are associated with a decrease in malonyl-CoA levels due to an increase in 5'-AMP-activated protein kinase inhibition of acetyl-CoA carboxylase.缺血性心脏再灌注期间脂肪酸氧化率高与丙二酰辅酶A水平降低有关，这是由于5'-AMP激活的蛋白激酶对乙酰辅酶A羧化酶的抑制作用增强所致。
J Biol Chem. 1995 Jul 21;270(29):17513-20. doi: 10.1074/jbc.270.29.17513.