Relevance of Endoplasmic Reticulum Stress Cell Signaling in Liver Cold Ischemia Reperfusion Injury.
Relevance of Endoplasmic Reticulum Stress Cell Signaling in Liver Cold Ischemia Reperfusion Injury.
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DOI：
10.3390/ijms17060807
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发表时间：
2016-05-25
影响因子：
5.6
通讯作者：
Roselló-Catafau J
中科院分区：
文献类型：
--
作者：
Folch-Puy E;Panisello A;Oliva J;Lopez A;Castro Benítez C;Adam R;Roselló-Catafau J
内质网(ER)参与钙稳态、蛋白质折叠和脂质生物合成。其正常功能的扰动会导致内质网应激(ERS)。这可以由许多生理病理条件触发，如酒精性脂肪性肝炎、胰岛素抵抗或缺血再灌注损伤。细胞通过启动称为未折叠蛋白反应(UPR)的防御过程来对ERS做出反应，该过程包括细胞适应和保护细胞生存的机制，或者在过度严重的应激情况下启动细胞死亡程序。最近的实验数据表明，ERS参与了移植肝的缺血/再灌注损伤(IRI)，这被认为是影响肝移植后预后的主要问题之一。本文就ERS/UPR的分子机制及其后果进行综述，重点介绍实体器官保存和肝移植模型的研究进展。我们还将讨论ERS的潜在作用，除了简单的适应性反应和细胞死亡的调节之外，在细胞功能属性和表型变化的改变中。
The endoplasmic reticulum (ER) is involved in calcium homeostasis, protein folding and lipid biosynthesis. Perturbations in its normal functions lead to a condition called endoplasmic reticulum stress (ERS). This can be triggered by many physiopathological conditions such as alcoholic steatohepatitis, insulin resistance or ischemia-reperfusion injury. The cell reacts to ERS by initiating a defensive process known as the unfolded protein response (UPR), which comprises cellular mechanisms for adaptation and the safeguarding of cell survival or, in cases of excessively severe stress, for the initiation of the cell death program. Recent experimental data suggest the involvement of ERS in ischemia/reperfusion injury (IRI) of the liver graft, which has been considered as one of major problems influencing outcome after liver transplantation. The purpose of this review is to summarize updated data on the molecular mechanisms of ERS/UPR and the consequences of this pathology, focusing specifically on solid organ preservation and liver transplantation models. We will also discuss the potential role of ERS, beyond the simple adaptive response and the regulation of cell death, in the modification of cell functional properties and phenotypic changes.