Potential Roles of Mitochondria-Associated ER Membranes (MAMs) in Traumatic Brain Injury
Potential Roles of Mitochondria-Associated ER Membranes (MAMs) in Traumatic Brain Injury
复制标题
线粒体相关内质网膜 (MAM) 在创伤性脑损伤中的潜在作用
DOI：
10.1007/s10571-017-0484-2
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发表时间：
2017-03
影响因子：
4
通讯作者：
Zhang Jianning
中科院分区：
文献类型：
--
作者：
Sun Dongdong;Chen Xin;Gu Gang;Wang Jianhao;Zhang Jianning
内质网（ER）和线粒体都被证明是至关重要的细胞内稳态。ER和线粒体的功能是相互独立的，但又相互关联。这两个细胞器可以形成物理相互作用，称为MAMs，以调节ER和线粒体之间的生理功能，以维持Ca 2+，脂质和代谢物交换。几种蛋白质位于MAMs中，包括RNA依赖性蛋白激酶（PKR）样ER激酶、肌醇1，4，5-三磷酸受体、磷酸弗林酸性簇分选蛋白-2和sigma-1受体以确保调节。最近的研究表明MAMs在各种情况下参与炎症和凋亡。所有这些功能在确定创伤性脑损伤（TBI）后的细胞命运中至关重要。我们假设MAMs可能与TBI相关，并可能导致线粒体功能障碍、ER应激、自噬失调、Ca 2+稳态失调和氧化应激。本文就MAM的形成及其在TBI病理生理中的调节作用作一综述。
The endoplasmic reticulum (ER) and mitochondria have both been shown to be critical in cellular homeostasis. The functions of the ER and mitochondria are independent but interrelated. These two organelles could form physical interactions, known as MAMs, to regulate physiological functions between ER and mitochondria to maintain Ca2+, lipid, and metabolite exchange. Several proteins are located in MAMs, including RNA-dependent protein kinase (PKR)-like ER kinase, inositol 1,4,5-trisphosphate receptors, phosphofurin acidic cluster sorting protein-2 and sigma-1 receptor to ensure regulation. Recent studies indicated that MAMs participate in inflammation and apoptosis in various conditions. All of these functions are crucial in determining cell fate following traumatic brain injury (TBI). We hypothesized that MAMs may associate with TBI and could contribute to mitochondrial dysfunction, ER stress, autophagy dysregulation, dysregulation of Ca2+homeostasis, and oxidative stress. In this review, we summarize the latest understanding of MAM formation and their potential regulatory role in TBI pathophysiology.
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影响因子：
82.9
作者：
通讯作者：
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影响因子：
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作者：
Schulman, Jacqualyn J.;Wright, Forrest A.;Wojcikiewicz, Richard J. H.
通讯作者：
Wojcikiewicz, Richard J. H.
影响因子：
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作者：
Schulman, Jacqualyn J.;Wright, Forrest A.;Wojcikiewicz, Richard J. H.
通讯作者：
Wojcikiewicz, Richard J. H.
影响因子：
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通讯作者：
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