线粒体病理生理学、活性氧与心血管疾病
Mitochondrial pathophysiology, reactive oxygen species, and cardiovascular diseases.
作者信息
Gao Ling, Laude Karine, Cai Hua
机构信息
Division of Molecular Medicine, Department of Anesthesiology, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
出版信息
Vet Clin North Am Small Anim Pract. 2008 Jan;38(1):137-55, vi. doi: 10.1016/j.cvsm.2007.10.004.
Abstract
This article discusses mitochondrial pathophysiology, reactive oxygen species, and cardiovascular diseases. Mitochondrial respiratory chains are responsible for energy metabolism/ATP production through the tricyclic antidepressant cycle, coupling of oxidative phosphorylation, and electron transfer. The mitochondrion produces reactive oxygen species as "side products" of respiration. The mitochondrial derived reactive oxygen species is involved in the pathogenesis of various clinical disorders including heart failure, hypoxia, ischemia/reperfusion injury, diabetes, neurodegenerative diseases, and the physiologic process of aging. Observational and mechanistical studies of these pathologic roles of mitochondria are discussed in depth in this article.
摘要
本文讨论了线粒体病理生理学、活性氧与心血管疾病。线粒体呼吸链通过三环抗抑郁药循环、氧化磷酸化偶联和电子传递负责能量代谢/三磷酸腺苷（ATP）生成。线粒体作为呼吸的“副产品”产生活性氧。线粒体衍生的活性氧参与包括心力衰竭、缺氧、缺血/再灌注损伤、糖尿病、神经退行性疾病等各种临床病症的发病机制以及衰老的生理过程。本文深入讨论了线粒体这些病理作用的观察性和机制性研究。
相似文献
1
Mitochondrial pathophysiology, reactive oxygen species, and cardiovascular diseases.线粒体病理生理学、活性氧与心血管疾病
Vet Clin North Am Small Anim Pract. 2008 Jan;38(1):137-55, vi. doi: 10.1016/j.cvsm.2007.10.004.
2
Mitochondrial Proton Leak Plays a Critical Role in Pathogenesis of Cardiovascular Diseases.线粒体质子泄漏在心血管疾病发病机制中起关键作用。
Adv Exp Med Biol. 2017;982:359-370. doi: 10.1007/978-3-319-55330-6_20.
3
Mitochondrial Reactive Oxygen Species Mediate Cardiac Structural, Functional, and Mitochondrial Consequences of Diet-Induced Metabolic Heart Disease.线粒体活性氧介导饮食诱导的代谢性心脏病的心脏结构、功能及线粒体改变
J Am Heart Assoc. 2016 Jan 11;5(1):e002555. doi: 10.1161/JAHA.115.002555.
4
Oxidative stress precedes skeletal muscle mitochondrial dysfunction during experimental aortic cross-clamping but is not associated with early lung, heart, brain, liver, or kidney mitochondrial impairment.在实验性主动脉交叉钳夹过程中，氧化应激先于骨骼肌线粒体功能障碍出现，但与早期肺、心脏、脑、肝脏或肾脏线粒体损伤无关。
J Vasc Surg. 2014 Oct;60(4):1043-51.e5. doi: 10.1016/j.jvs.2013.07.100. Epub 2013 Oct 3.
5
Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion.电子传递的调节可保护心脏线粒体并减少缺血再灌注期间的心肌损伤。
Am J Physiol Cell Physiol. 2007 Jan;292(1):C137-47. doi: 10.1152/ajpcell.00270.2006. Epub 2006 Sep 13.
6
Humanin exerts cardioprotection against cardiac ischemia/reperfusion injury through attenuation of mitochondrial dysfunction.人胰岛素通过减轻线粒体功能障碍对心脏缺血/再灌注损伤发挥心脏保护作用。
Cardiovasc Ther. 2016 Dec;34(6):404-414. doi: 10.1111/1755-5922.12210.
7
Mitochondria-Targeted Antioxidants for the Treatment of Cardiovascular Disorders.用于治疗心血管疾病的线粒体靶向抗氧化剂
Adv Exp Med Biol. 2017;982:621-646. doi: 10.1007/978-3-319-55330-6_32.
8
Cardiac mitochondria and reactive oxygen species generation.心脏线粒体和活性氧物质的产生。
Circ Res. 2014 Jan 31;114(3):524-37. doi: 10.1161/CIRCRESAHA.114.300559.
9
Mitochondrial inefficiencies and anoxic ATP hydrolysis capacities in diabetic rat heart.糖尿病大鼠心脏中线粒体效率低下和缺氧 ATP 水解能力。
Am J Physiol Cell Physiol. 2014 Sep 15;307(6):C499-507. doi: 10.1152/ajpcell.00006.2014. Epub 2014 Jun 11.
10
The breathing heart - mitochondrial respiratory chain dysfunction in cardiac disease.呼吸的心脏——心脏疾病中线粒体呼吸链功能障碍。
Int J Cardiol. 2014 Feb 1;171(2):134-43. doi: 10.1016/j.ijcard.2013.12.014. Epub 2013 Dec 18.
引用本文的文献
1
Piperine Induces Apoptosis and Cell Cycle Arrest via Multiple Oxidative Stress Mechanisms and Regulation of PI3K/Akt and MAPK Signaling in Colorectal Cancer Cells.胡椒碱通过多种氧化应激机制以及对PI3K/Akt和MAPK信号通路的调控诱导结肠癌细胞凋亡和细胞周期停滞。
Antioxidants (Basel). 2025 Jul 21;14(7):892. doi: 10.3390/antiox14070892.
2
Unravelling the Connection Between Energy Metabolism and Immune Senescence/Exhaustion in Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.揭示肌痛性脑脊髓炎/慢性疲劳综合征患者能量代谢与免疫衰老/耗竭之间的联系。
Biomolecules. 2025 Mar 1;15(3):357. doi: 10.3390/biom15030357.
3
The role of Tyr34 in proton coupled electron transfer and product inhibition of manganese superoxide dismutase.酪氨酸34在质子耦合电子转移及锰超氧化物歧化酶产物抑制中的作用
Nat Commun. 2025 Feb 22;16(1):1887. doi: 10.1038/s41467-025-57180-3.
4
Metabolic rewiring in fat-depleted Drosophila reveals triglyceride:glycogen crosstalk and identifies cDIP as a new regulator of energy metabolism.脂肪耗尽的果蝇中的代谢重编程揭示了甘油三酯与糖原的相互作用，并将cDIP鉴定为能量代谢的新调节因子。
Res Sq. 2024 Oct 18:rs.3.rs-4505077. doi: 10.21203/rs.3.rs-4505077/v1.
5
Revealing the atomic and electronic mechanism of human manganese superoxide dismutase product inhibition.揭示人锰超氧化物歧化酶产物抑制的原子和电子机制。
Nat Commun. 2024 Jul 16;15(1):5973. doi: 10.1038/s41467-024-50260-w.
6
Potential Role of Dipeptidyl Peptidase-4 in Regulating Mitochondria and Oxidative Stress in Cardiomyocytes.二肽基肽酶-4 在调节心肌细胞线粒体和氧化应激中的潜在作用。
Cardiovasc Toxicol. 2024 Oct;24(10):1090-1104. doi: 10.1007/s12012-024-09884-z. Epub 2024 Jul 2.
7
The role of Tyr34 in proton-coupled electron transfer of human manganese superoxide dismutase.酪氨酸34在人锰超氧化物歧化酶质子耦合电子转移中的作用。
Res Sq. 2024 Jun 11:rs.3.rs-4494128. doi: 10.21203/rs.3.rs-4494128/v1.
8
Revealing the atomic and electronic mechanism of human manganese superoxide dismutase product inhibition.揭示人类锰超氧化物歧化酶产物抑制的原子和电子机制。
Res Sq. 2024 Feb 5:rs.3.rs-3880128. doi: 10.21203/rs.3.rs-3880128/v1.
9
Hemoglobin Subunit Theta 1 Promotes Proliferation by Reducing Reactive Oxygen Species in Lung Adenocarcinoma.血红蛋白亚基θ1通过降低肺腺癌中的活性氧来促进增殖。
Cancers (Basel). 2023 Nov 21;15(23):5504. doi: 10.3390/cancers15235504.
10
Activation of PI3K/Akt mediates the protective effect of diallyl trisulfide on doxorubicin induced cardiac apoptosis.PI3K/Akt的激活介导了二烯丙基三硫对阿霉素诱导的心脏细胞凋亡的保护作用。
Curr Res Toxicol. 2023 Nov 11;5:100136. doi: 10.1016/j.crtox.2023.100136. eCollection 2023.
本文引用的文献
1
Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury.线粒体在暴露于实验性缺血再灌注损伤的心肌样细胞和离体心脏中传递凋亡信号。
Redox Rep. 2007;12(3):148-62. doi: 10.1179/135100007X200227.
2
The late phase of ischemic preconditioning induces a prosurvival genetic program that results in marked attenuation of apoptosis.缺血预处理的晚期阶段诱导一种促生存基因程序，从而导致细胞凋亡显著减少。
J Mol Cell Cardiol. 2007 Jun;42(6):1075-85. doi: 10.1016/j.yjmcc.2007.03.908. Epub 2007 Apr 4.
3
Endothelial mitochondria: contributing to vascular function and disease.内皮线粒体：对血管功能和疾病的影响
Circ Res. 2007 Apr 27;100(8):1128-41. doi: 10.1161/01.RES.0000261970.18328.1d.
4
Oxidative stress, mitochondrial DNA mutation, and apoptosis in aging.衰老过程中的氧化应激、线粒体DNA突变与细胞凋亡。
Exp Biol Med (Maywood). 2007 May;232(5):592-606.
5
Thioredoxins, mitochondria, and hypertension.硫氧还蛋白、线粒体与高血压
Am J Pathol. 2007 Mar;170(3):805-8. doi: 10.2353/ajpath.2007.061243.
6
Deficiency of glutathione peroxidase-1 accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice.谷胱甘肽过氧化物酶-1缺乏会加速载脂蛋白E缺乏小鼠的动脉粥样硬化进程。
Arterioscler Thromb Vasc Biol. 2007 Apr;27(4):850-7. doi: 10.1161/01.ATV.0000258809.47285.07. Epub 2007 Jan 25.
7
The cellular basis for diverse responses to oxygen.对氧气产生多种反应的细胞基础。
Free Radic Biol Med. 2007 Jan 15;42(2):165-74. doi: 10.1016/j.freeradbiomed.2006.10.048. Epub 2006 Oct 28.
8
Arrhythmia and neuronal/endothelial myocyte uncoupling in hyperhomocysteinemia.高同型半胱氨酸血症中的心律失常以及神经元/内皮细胞与心肌细胞解偶联
Arch Physiol Biochem. 2006 Oct-Dec;112(4-5):219-27. doi: 10.1080/13813450601093443.
9
Ceramide induces early and late apoptosis in human papilloma virus+ cervical cancer cells by inhibiting reactive oxygen species decay, diminishing the intracellular concentration of glutathione and increasing nuclear factor-kappaB translocation.神经酰胺通过抑制活性氧的衰减、降低细胞内谷胱甘肽浓度以及增加核因子-κB易位，诱导人乳头瘤病毒阳性宫颈癌细胞发生早期和晚期凋亡。
Anticancer Drugs. 2007 Feb;18(2):149-59. doi: 10.1097/CAD.0b013e3280115111.
10
The thioredoxin system in cancer.癌症中的硫氧还蛋白系统。
Semin Cancer Biol. 2006 Dec;16(6):420-6. doi: 10.1016/j.semcancer.2006.10.009. Epub 2006 Oct 28.
Zotero 插件