It is now increasingly recognized that endoplasmic reticulum (ER) stress, which is caused by the accumulation of overproduced or misfolded proteins in this organelle, contributes to the pathogenesis of a diverse range of human diseases. ER stress initiates the unfolded protein response (UPR) in an attempt to restore cellular protein homeostasis and promote cell survival. However, when ER stress is severe or protracted, and uncompensated, the UPR can fail, resulting in cell death, often by apoptosis. ER stress has received relatively little attention in the veterinary literature and the intent of this mini review is to describe the essential features of ER stress and UPR in determining the survival or demise of an affected cell and encourage further study of its role in the pathogenesis of diseases of domestic animal species. The role of ER stress, particularly when chronic and unrelieved, in the pathogenesis of a number of specific diseases is also discussed.

现在人们越来越认识到，内质网 (ER) 应激是由该细胞器中过度生产或错误折叠的蛋白质积累引起的，有助于多种人类疾病的发病机制。内质网应激启动未折叠蛋白反应 (UPR)，试图恢复细胞蛋白稳态并促进细胞存活。然而，当内质网应激严重或长期且未代偿时，UPR 可能会失败，导致细胞死亡，通常是由于细胞凋亡。内质网应激在兽医文献中受到的关注相对较少，本次小型综述的目的是描述内质网应激和 UPR 在决定受影响细胞的存活或死亡方面的基本特征，并鼓励进一步研究其在发病机制中的作用。家畜物种的疾病。ER应激的作用，