细胞会激活保护机制来克服威胁细胞内稳态的压力情况，包括钙、氧化还原和营养物水平的失衡。内质网（ER）压力会激活细胞内信号通路，即未折叠蛋白质应答（UPR），以缓解这种情况并保护细胞。尽管ER压力有时是自噬的负调节因子，但ER压力诱导的UPR通常会激活自噬，这是一种自我降解的途径，进一步支持其细胞保护作用。持续激活ER压力和自噬会引发细胞死亡，并被视为某些疾病的治疗靶点。然而，ER压力诱导的自噬也可能导致肿瘤治疗耐药和某些疾病恶化。由于ER压力应答和自噬会相互影响，而它们的激活程度与各种疾病密切相关，因此了解它们的关系非常重要。在本文中，我们总结了两种基本的细胞应激反应，即ER压力应答和自噬，以及它们在病理条件下的相互作用，以帮助开发治疗炎症性疾病、神经退行性疾病和癌症的方法。 © 2023作者。由Informa UK Limited出版，交易为Taylor＆Francis Group。

Cells activate protective mechanisms to overcome stressful conditions that threaten cellular homeostasis, including imbalances in calcium, redox, and nutrient levels. Endoplasmic reticulum (ER) stress activates an intracellular signaling pathway, known as the unfolded protein response (UPR), to mitigate such circumstances and protect cells. Although ER stress is sometimes a negative regulator of autophagy, UPR induced by ER stress typically activates autophagy, a self-degradative pathway that further supports its cytoprotective role. Sustained activation of ER stress and autophagy is known to trigger cell death and is considered a therapeutic target for certain diseases. However, ER stress-induced autophagy can also lead to treatment resistance in cancer and exacerbation of certain diseases. Since the ER stress response and autophagy affect each other, and the degree of their activation is closely related to various diseases, understanding their relationship is very important. In this review, we summarize the current understanding of two fundamental cellular stress responses, the ER stress response and autophagy, and their crosstalk under pathological conditions to help develop therapies for inflammatory diseases, neurodegenerative disorders, and cancer.© 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.