کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8298558 | 1537030 | 2018 | 34 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mitochondrial uncoupling, ROS generation and cardioprotection
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کلمات کلیدی
DNPGSISUCPHNECCCPIPCΔΨmFCCPPPARαCCOANTδpΔpHNrf22,4-Dinitrophenol - 2،4-دینیتروفنل4-hydroxy-2-nonenal - 4-هیدروکسی-2 غیرنالischemic preconditioning - preconditioning ایسکمیکROS - ROSMitochondrial uncoupling - انحلال میتوکندریاییischemia-reperfusion - ایسکمی-رپرفیوژنadenine nucleotide translocator - ترجمه آدنین نوکلئوتیدیGlucose-stimulated insulin secretion - ترشح انسولین تحریک شده توسط گلوکزCardioprotection - حفاظت از قلبRET - حقcytochrome c oxidase - سیتوکروم سی اکسیدازnuclear factor erythroid 2-related factor 2 - فاکتور هسته ای عامل erythroid 2 مرتبط 2reverse electron transport - معکوس حمل و نقل الکترونProton leak - نشت پروتونProtonmotive force - نیروی ProtonmotoMitochondrial membrane potential - پتانسیل غشای میتوکندریUncoupling protein - پروتئین جدا کردنcarbonyl cyanide m-chlorophenylhydrazone - کربنیل سیانید m-chlorophenylhydrazonecarbonyl cyanide p-trifluoromethoxyphenylhydrazone - کربونیل سیانید p-trifluoromethoxyphenylhydrazoneReactive oxygen species (ROS) - گونه های اکسیژن واکنشی (ROS)Reactive oxygen species - گونههای فعال اکسیژنperoxisome proliferator-activated receptor α - گیرنده پروتئینی فعال پروکسایزوم α
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
دانش گیاه شناسی
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چکیده انگلیسی
Mitochondrial oxidative phosphorylation is incompletely coupled, since protons translocated to the intermembrane space by specific respiratory complexes of the electron transport chain can return to the mitochondrial matrix independently of the ATP synthase -a process known as proton leak- generating heat instead of ATP. Proton leak across the inner mitochondrial membrane increases the respiration rate and decreases the electrochemical proton gradient (Îp), and is an important mechanism for energy dissipation that accounts for up to 25% of the basal metabolic rate. It is well established that mitochondrial superoxide production is steeply dependent on Îp in isolated mitochondria and, correspondingly, mitochondrial uncoupling has been identified as a cytoprotective strategy under conditions of oxidative stress, including diabetes, drug-resistance in tumor cells, ischemia-reperfusion (IR) injury or aging. Mitochondrial uncoupling proteins (UCPs) are able to lower the efficiency of oxidative phosphorylation and are involved in the control of mitochondrial reactive oxygen species (ROS) production. There is strong evidence that UCP2 and UCP3, the UCP1 homologues expressed in the heart, protect against mitochondrial oxidative damage by reducing the production of ROS. This review first analyzes the relationship between mitochondrial proton leak and ROS generation, and then focuses on the cardioprotective role of chemical uncoupling and uncoupling mediated by UCPs. This includes their protective effects against cardiac IR, a condition known to increase ROS production, and their roles in modulating cardiovascular risk factors such as obesity, diabetes and atherosclerosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Bioenergetics - Volume 1859, Issue 9, September 2018, Pages 940-950
Journal: Biochimica et Biophysica Acta (BBA) - Bioenergetics - Volume 1859, Issue 9, September 2018, Pages 940-950
نویسندگان
Susana Cadenas,