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线粒体药理学:现在是它的未来。

Mitochondrial pharmacology: its future is now.

机构信息

Department of Pharmacology, Joan and Sanford I. Weill Medical College of Cornell University, New York, New York, USA.

Department of Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital, Little Rock, Arkansas, USA.

出版信息

Clin Pharmacol Ther. 2014 Dec;96(6):629-33. doi: 10.1038/clpt.2014.177.

DOI:10.1038/clpt.2014.177
PMID:25399706
Abstract

Mitochondrial medicine is an evolving discipline whose importance derives from the central function of mitochondria in adenosine triphosphate (ATP) production, generation of reactive oxygen species, and cell death by necrosis or apoptosis. Consequently, mitochondrial dysfunction plays an important role in the progression of aging and the pathophysiology of many common diseases and off-target drug effects. This provides an impetus for the development of mitochondrial pharmacology, and some promising therapeutic targets for mitochondrial protective therapy have been identified.

摘要

线粒体医学是一门不断发展的学科,其重要性源于线粒体在三磷酸腺苷(ATP)生成、活性氧产生以及通过坏死或细胞凋亡导致细胞死亡中的核心功能。因此,线粒体功能障碍在衰老的进展和许多常见疾病的病理生理学以及药物的脱靶效应中起着重要作用。这为线粒体药理学的发展提供了动力,并且已经确定了一些有希望的线粒体保护治疗的治疗靶点。

相似文献

1
Mitochondrial pharmacology: its future is now.线粒体药理学:现在是它的未来。
Clin Pharmacol Ther. 2014 Dec;96(6):629-33. doi: 10.1038/clpt.2014.177.
2
[Mitochondria in cell life, death and disease].[细胞生命、死亡及疾病中的线粒体]
Postepy Biochem. 2008;54(2):129-41.
3
Mitochondria: the hemi of the cell.线粒体:细胞的“半壁江山” 。 (此翻译尽量贴合字面意思,但原英文表述比较奇特,正常可能说“Mitochondria: the powerhouses of the cell.” 线粒体:细胞的动力工厂 )
Adv Emerg Nurs J. 2009 Jan-Mar;31(1):54-62. doi: 10.1097/TME.0b013e3181956200.
4
Mitochondrial function and dysfunction: an update.线粒体功能和障碍:更新。
J Pharmacol Exp Ther. 2012 Sep;342(3):598-607. doi: 10.1124/jpet.112.192104. Epub 2012 Jun 13.
5
Mitochondria-dependent reactive oxygen species-mediated programmed cell death induced by 3,3'-diindolylmethane through inhibition of F0F1-ATP synthase in unicellular protozoan parasite Leishmania donovani.3,3'-二吲哚基甲烷通过抑制单细胞原生动物寄生虫杜氏利什曼原虫中的F0F1 - ATP合酶诱导线粒体依赖性活性氧介导的程序性细胞死亡。
Mol Pharmacol. 2008 Nov;74(5):1292-307. doi: 10.1124/mol.108.050161. Epub 2008 Aug 14.
6
Targeting autophagy and mitophagy for mitochondrial diseases treatment.针对线粒体疾病治疗的自噬和线粒体自噬靶向治疗。
Expert Opin Ther Targets. 2016;20(4):487-500. doi: 10.1517/14728222.2016.1101068. Epub 2015 Nov 2.
7
[Endothelial mitochondria--a novel target for pharmacology of endothelial dysfunction].[内皮线粒体——内皮功能障碍药理学的新靶点]
Postepy Biochem. 2008;54(2):198-208.
8
Mitochondrial functionality in reproduction: from gonads and gametes to embryos and embryonic stem cells.生殖中的线粒体功能:从性腺、配子到胚胎及胚胎干细胞
Hum Reprod Update. 2009 Sep-Oct;15(5):553-72. doi: 10.1093/humupd/dmp016. Epub 2009 May 4.
9
Caffeine increases mitochondrial function and blocks melatonin signaling to mitochondria in Alzheimer's mice and cells.咖啡因可增加线粒体功能并阻断阿尔茨海默病小鼠和细胞中线粒体的褪黑素信号传导。
Neuropharmacology. 2012 Dec;63(8):1368-79. doi: 10.1016/j.neuropharm.2012.08.018. Epub 2012 Sep 1.
10
Nicotinamide pretreatment protects cardiomyocytes against hypoxia-induced cell death by improving mitochondrial stress.烟酰胺预处理通过改善线粒体应激保护心肌细胞免受缺氧诱导的细胞死亡。
Pharmacology. 2012;90(1-2):11-8. doi: 10.1159/000338628. Epub 2012 Jun 14.

引用本文的文献

1
Pharmacological modulation of mitochondrial ion channels.线粒体离子通道的药理学调节。
Br J Pharmacol. 2019 Nov;176(22):4258-4283. doi: 10.1111/bph.14544. Epub 2019 Jan 2.
2
Exploring the Process of Energy Generation in Pathophysiology by Targeted Metabolomics: Performance of a Simple and Quantitative Method.通过靶向代谢组学探索病理生理学中的能量生成过程:一种简单定量方法的性能
J Am Soc Mass Spectrom. 2016 Jan;27(1):168-77. doi: 10.1007/s13361-015-1262-3. Epub 2015 Sep 17.
3
Microglial cell dysregulation in brain aging and neurodegeneration.
脑衰老和神经退行性变中的小胶质细胞失调。
Front Aging Neurosci. 2015 Jul 20;7:124. doi: 10.3389/fnagi.2015.00124. eCollection 2015.
4
Abnormal Glucose Metabolism in Alzheimer's Disease: Relation to Autophagy/Mitophagy and Therapeutic Approaches.阿尔茨海默病中的异常葡萄糖代谢:与自噬/线粒体自噬的关系及治疗方法
Neurochem Res. 2015 Dec;40(12):2557-69. doi: 10.1007/s11064-015-1631-0. Epub 2015 Jun 16.