The Uncoupling Proteins: A Systematic Review on the Mechanism Used in the Prevention of Oxidative Stress.
The Uncoupling Proteins: A Systematic Review on the Mechanism Used in the Prevention of Oxidative Stress.
复制标题
解偶联蛋白：氧化应激预防机制的系统综述。
DOI：
10.3390/antiox11020322
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发表时间：
2022-02-06
期刊：
影响因子：
--
通讯作者：
Mailloux RJ
中科院分区：
文献类型：
--
作者：
Hirschenson J;Melgar-Bermudez E;Mailloux RJ
线粒体解偶联蛋白（UCP） 1-3具有多种生理功能，包括非寒战产热（UCP1）、葡萄糖刺激胰岛素释放（GSIS）、饱腹感信号（UCP2）和肌肉燃料代谢（UCP3）。一些研究表明ucp通过促进质子返回基质来调节这些功能。这将降低呼吸链上的质子背压，降低第二个信使过氧化氢（H2O2）的产生。然而，通过激活这些蛋白质的泄漏来控制线粒体H2O2的产生以防止氧化应激仍然存在激烈的争论。这是由于令人信服的证据表明UCP2/3具有其他功能，并且无法重现UCP1-3使用诱导泄漏来控制活性氧（ROS）产生的发现。此外，其他研究发现UCP2/3可能作为Ca2+。因此，我们进行了一项系统综述，旨在总结收集到的关于该主题的结果。利用Pubmed、BIOSIS引文索引和Scopus中的精选关键词列表进行文献检索。筛选可能相关的文献，剔除重复的文献，然后使用Rayyan软件对文献标题和摘要进行评价。共有1101项符合条件的研究被纳入本综述。根据纳入标准，共对416项研究进行了评估。总的来说，大多数研究确定了ucp在预防氧化应激中的作用，在某些情况下，这可能与诱导泄漏和降低呼吸链上的质子背压有关。然而，一些研究也证明UCP2/3可能通过将Ca2+运输到基质中，输出脂质氢过氧化物或运输C-4代谢物来减轻氧化应激。此外，一些研究表明，激活UCP1或3可以增加线粒体ROS的产生，尽管仍然增强了对氧化应激的保护。结论：总的来说，大多数现有的研究表明UCPs，特别是UCP2/3，可以预防氧化应激。然而，用于这样做的机制仍然难以捉摸，并提出了UCP2/3应该重新命名的问题，因为它们可能仍然不是真正的“解偶联蛋白”。
Mitochondrial uncoupling proteins (UCP) 1-3 fulfill many physiological functions, ranging from non-shivering thermogenesis (UCP1) to glucose-stimulated insulin release (GSIS) and satiety signaling (UCP2) and muscle fuel metabolism (UCP3). Several studies have suggested that UCPs mediate these functions by facilitating proton return to the matrix. This would decrease protonic backpressure on the respiratory chain, lowering the production of hydrogen peroxide (H2O2), a second messenger. However, controlling mitochondrial H2O2 production to prevent oxidative stress by activating these leaks through these proteins is still enthusiastically debated. This is due to compelling evidence that UCP2/3 fulfill other function(s) and the inability to reproduce findings that UCP1-3 use inducible leaks to control reactive oxygen species (ROS) production. Further, other studies have found that UCP2/3 may serve as Ca2+. Therefore, we performed a systematic review aiming to summarize the results collected on the topic. A literature search using a list of curated keywords in Pubmed, BIOSIS Citation Index and Scopus was conducted. Potentially relevant references were screened, duplicate references eliminated, and then literature titles and abstracts were evaluated using Rayyan software. A total of 1101 eligible studies were identified for the review. From this total, 416 studies were evaluated based on our inclusion criteria. In general, most studies identified a role for UCPs in preventing oxidative stress, and in some cases, this may be related to the induction of leaks and lowering protonic backpressure on the respiratory chain. However, some studies also generated evidence that UCP2/3 may mitigate oxidative stress by transporting Ca2+ into the matrix, exporting lipid hydroperoxides, or by transporting C-4 metabolites. Additionally, some showed that activating UCP1 or 3 can increase mitochondrial ROS production, even though there is still augmented protection from oxidative stress. Conclusion: Overall, most available studies demonstrate that UCPs, particularly UCP2/3, prevent oxidative stress. However, the mechanism utilized to do so remains elusive and raises the question that UCP2/3 should be renamed, since they may still not be true “uncoupling proteins”.
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DOI：
10.1074/jbc.m110.216044
发表时间：
2011-09-16
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
De Marchi U;Castelbou C;Demaurex N
通讯作者：
Demaurex N
影响因子：
16.6
作者：
Madreiter-Sokolowski, Corina T.;Klec, Christiane;Parichatikanond, Warisara;Stryeck, Sarah;Gottschalk, Benjamin;Pulido, Sergio;Rost, Rene;Eroglu, Emrah;Hofmann, Nicole A.;Bondarenko, Alexander I.;Madl, Tobias;Waldeck-Weiermair, Markus;Malli, Roland;Graier, Wolfgang F.
通讯作者：
Graier, Wolfgang F.
影响因子：
4.1
作者：
Affourtit, Charles;Brand, Martin D.
通讯作者：
Brand, Martin D.
影响因子：
4.8
作者：
NegreSalvayre, A;Hirtz, C;Casteilla, L
通讯作者：
Casteilla, L
影响因子：
64.8
作者：
Chouchani ET;Kazak L;Jedrychowski MP;Lu GZ;Erickson BK;Szpyt J;Pierce KA;Laznik-Bogoslavski D;Vetrivelan R;Clish CB;Robinson AJ;Gygi SP;Spiegelman BM
通讯作者：
Spiegelman BM