24 、Leigh syndrome is a severe early-onset progressive neurodegenerative disorder due tomitochondrialoxidative phosphorylation defects.───Leigh综合征是一种由于线粒体氧化**酸化障碍所导致的严重退行性脑病。 25 、And now having gotten the results, we can see there's some evidence ofmitochondrialactivit...
3. NecroX-5 protects mitochondrial oxidative phosphorylation capacity and preserves PGC1α expression levels during hypoxia/reoxygenation injury [J] . Thu Vu Thi, Kim Hyoung Kyu, Long Le Thanh, The Korean Journal of Physiology & Pharmacology . 2016,第2期 机译:NecroX-5在缺氧/复氧损伤...
For this reason, the expression of mtDNA is vital forthe assembly and functioning of the oxidative phosphorylation complexes. Defects of themechanisms regulating mtDNA gene expression have been associated with def i cienciesin assembly of these complexes, resulting in mitochondrial diseases. Recently, ...
例如, 抑制Drp1表达可促使线粒体延长, 导致氧化磷酸化(oxidative phosphorylation, OXPHOS)复合物Ⅳ活力下降, ATP合成受阻[43]. 在出现线粒体碎裂的细胞中, 线粒体钙离子吸收能力和线粒体内钙离子扩散能力均有下降, 说明线粒体动态平衡异常影响钙离子稳态[44,45]. 还有证据显示, 线粒体形态变化与OXPHOS复合物的...
Damage to Mitochondrial DNA disrupts Mitochondrial oxidative phosphorylation, contributing to a number of Human diseases (Ref. 5 6). Following the reception of stress signals, proapoptotic Bcl2 family proteins are activated and subsequently interact with and inactivate antiapoptotic Bcl2 proteins. Bcl2 ...
ETC function is coupled to the generation of ATP-that is, oxidative phosphorylation and the production of metabolites by the tricarboxylic acid (TCA) cycle. Mitochondrial complexes I and II donate electrons to ubiquinone, resulting in the generation of ubiquinol and the regeneration of the NAD+ ...
The mitochondrial brown fat uncoupling protein 1 (UCP1) is a member of the family of mitochondrial anion carrier proteins (MACP). UCPs separate oxidative phosphorylation from ATP synthesis with energy dissipated as heat,also referred to as the mitochondrial proton leak. UCPs facilitate the transfer...
Complex I is the largest protein complex of the oxidative phosphorylation system in mitochondrial and it catalyzes NADH-quinone oxidoreduction. Complex I represents the main entrance site for electrons into the respiratory electron transfer chain. In Ara
Tomatidine treatment stimulated mitochondrial functions, including mitochondrial membrane potential, oxidative phosphorylation, and ATP production, in hESC-CMs. Tomatidine-treated hESC-CMs were more sensitive to doxorubicin-induced cardiotoxicity than the control cells. In conclusion, the present study ...