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瘦素的心血管作用。

Cardiovascular effects of leptin.

机构信息

Institut Pasteur Korea, Bundang-gu, Gyeonggi-do, Korea.

出版信息

Nat Rev Cardiol. 2010 Jan;7(1):22-9. doi: 10.1038/nrcardio.2009.224. Epub 2009 Dec 1.

DOI:10.1038/nrcardio.2009.224
PMID:19949425
Abstract

A wealth of investigations, ranging from clinical and animal model studies to in vitro analyses, have generated great interest in the cardiovascular effects of leptin. Accordingly, many studies have examined the contribution of leptin to cardiac remodeling in heart failure and whether the effects of leptin on metabolism, apoptosis, extracellular matrix remodeling, and hypertrophy could explain the so-called obesity paradox. Furthermore, obesity and hyperleptinemia have often been associated with hypertension, and regulation of sympathetic tone or direct effects of leptin on contributors such as atherosclerosis, endothelial dysfunction, and thrombosis have been documented. Unfortunately, translating basic research studies in vitro, or in animal models, to human physiology has proven difficult. The degree of leptin resistance in obesity is one intriguing issue that must be resolved. Furthermore, the importance of autocrine and paracrine effects of leptin derived from the heart and perivascular adipose tissue must be further studied. Carefully planned and executed research to conclusively establish distinct effects of leptin on the cardiovascular system in normal and diseased states will be essential to harness any therapeutic potential associated with leptin's effects.

摘要

大量的研究,包括临床和动物模型研究以及体外分析,都对瘦素的心血管效应产生了浓厚的兴趣。因此,许多研究都探讨了瘦素在心力衰竭中心脏重构中的作用,以及瘦素对代谢、细胞凋亡、细胞外基质重构和肥大的影响是否可以解释所谓的肥胖悖论。此外,肥胖和高瘦素血症通常与高血压有关,并且已经证明了瘦素对贡献者(如动脉粥样硬化、内皮功能障碍和血栓形成)的交感神经张力调节或直接作用。不幸的是,将体外或动物模型中的基础研究转化为人体生理学证明是困难的。肥胖患者的瘦素抵抗程度是一个需要解决的有趣问题。此外,还必须进一步研究来自心脏和血管周围脂肪组织的瘦素的自分泌和旁分泌作用。精心计划和执行的研究对于确定瘦素在正常和疾病状态下对心血管系统的明确影响至关重要,这将是利用瘦素相关作用的任何治疗潜力的关键。

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Leptin attenuates hypoxia/reoxygenation-induced activation of the intrinsic pathway of apoptosis in rat H9c2 cells.瘦素可减轻缺氧/复氧诱导的大鼠H9c2细胞凋亡内源性途径的激活。
J Cell Physiol. 2009 Nov;221(2):490-7. doi: 10.1002/jcp.21883.
2
Stimulation of cardiac fatty acid oxidation by leptin is mediated by a nitric oxide-p38 MAPK-dependent mechanism.瘦素对心脏脂肪酸氧化的刺激作用是由一种一氧化氮-p38丝裂原活化蛋白激酶依赖性机制介导的。
Eur J Pharmacol. 2009 Sep 1;617(1-3):113-7. doi: 10.1016/j.ejphar.2009.06.037. Epub 2009 Jun 30.
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Leptin and endothelin-1 mediated increased extracellular matrix protein production and cardiomyocyte hypertrophy in diabetic heart disease.
脂肪细胞因子及其对糖尿病患者心肌缺血/再灌注损伤易感性的潜在影响。
Lipids Health Dis. 2024 Nov 13;23(1):372. doi: 10.1186/s12944-024-02357-w.
4
miRNA and leptin signaling in metabolic diseases and at extreme environments.微小RNA与瘦素信号通路在代谢性疾病及极端环境中的作用
Pharmacol Res Perspect. 2024 Aug;12(4):e1248. doi: 10.1002/prp2.1248.
5
Metabolic Effects of Ketogenic Diets: Exploring Whole-Body Metabolism in Connection with Adipose Tissue and Other Metabolic Organs.生酮饮食的代谢效应:探究与脂肪组织和其他代谢器官相关的全身代谢。
Int J Mol Sci. 2024 Jun 27;25(13):7076. doi: 10.3390/ijms25137076.
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Mediators between body mass index and atrial fibrillation: a Mendelian randomization study.体重指数与心房颤动之间的中介因素:一项孟德尔随机化研究。
Front Nutr. 2024 May 22;11:1369594. doi: 10.3389/fnut.2024.1369594. eCollection 2024.
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Sodium-Glucose Cotransporter Protein 2 Inhibitors: Novel Application for the Treatment of Obesity-Associated Hypertension.钠-葡萄糖协同转运蛋白2抑制剂:治疗肥胖相关性高血压的新应用
Diabetes Metab Syndr Obes. 2024 Jan 26;17:407-415. doi: 10.2147/DMSO.S446904. eCollection 2024.
8
Atherosclerotic plaque development in mice is enhanced by myeloid ZEB1 downregulation.骨髓细胞中 ZEB1 的下调会增强小鼠动脉粥样硬化斑块的发展。
Nat Commun. 2023 Dec 14;14(1):8316. doi: 10.1038/s41467-023-43896-7.
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Gastrin attenuates sepsis-induced myocardial dysfunction by down-regulation of TLR4 expression in macrophages.胃泌素通过下调巨噬细胞中TLR4的表达减轻脓毒症诱导的心肌功能障碍。
Acta Pharm Sin B. 2023 Sep;13(9):3756-3769. doi: 10.1016/j.apsb.2023.06.012. Epub 2023 Jun 23.
10
Mechanisms and Outcomes of Metabolic Surgery in Type 2 Diabetes.2型糖尿病代谢手术的机制与结局
Metabolites. 2022 Nov 17;12(11):1134. doi: 10.3390/metabo12111134.
瘦素和内皮素-1介导糖尿病性心脏病中细胞外基质蛋白生成增加及心肌细胞肥大。
Diabetes Metab Res Rev. 2009 Jul;25(5):452-63. doi: 10.1002/dmrr.964.
4
The cardioprotective actions of leptin are lost in the Zucker obese (fa/fa) rat.在Zucker肥胖(fa/fa)大鼠中,瘦素的心脏保护作用丧失。
J Cardiovasc Pharmacol. 2009 Apr;53(4):311-7. doi: 10.1097/FJC.0b013e31819d6152.
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Apoptosis. 2009 Apr;14(4):536-48. doi: 10.1007/s10495-008-0302-x.
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Absence of leptin resistance in platelets from morbidly obese individuals may contribute to the increased thrombosis risk in obesity.病态肥胖个体血小板中不存在瘦素抵抗,这可能导致肥胖人群血栓形成风险增加。
Thromb Haemost. 2008 Dec;100(6):1123-9.