Wiese Wojciech, Galita Grzegorz, Siwecka Natalia, Rozpędek-Kamińska Wioletta, Slupianek Artur, Majsterek Ireneusz
Department of Clinical Chemistry and Biochemistry, Medical University of Lodz, Mazowiecka 5, 92-215 Lodz, Poland.
Office of the Vice President for Research, Temple University, Philadelphia, PA 19140, USA.
Int J Mol Sci. 2025 Mar 27;26(7):3092. doi: 10.3390/ijms26073092.
Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy that poses a significant therapeutic challenge due to its high recurrence rate and demanding treatment regimens. Increasing evidence suggests that endoplasmic reticulum (ER) stress and downstream activation of the unfolded protein response (UPR) pathway play a key role in the pathogenesis of AML. ER stress is triggered by the accumulation of misfolded or unfolded proteins within the ER. This causes activation of the UPR to restore cellular homeostasis. However, the UPR can shift from promoting survival to inducing apoptosis under prolonged or excessive stress conditions. AML cells can manipulate the UPR pathway to evade apoptosis, promoting tumor progression and resistance against various therapeutic strategies. This review provides the current knowledge on ER stress in AML and its prognostic and therapeutic implications.
急性髓系白血病（AML）是一种异质性血液系统恶性肿瘤，因其高复发率和严格的治疗方案而带来重大治疗挑战。越来越多的证据表明，内质网（ER）应激和未折叠蛋白反应（UPR）途径的下游激活在AML发病机制中起关键作用。ER应激由内质网内错误折叠或未折叠蛋白的积累引发。这导致UPR激活以恢复细胞稳态。然而，在长期或过度应激条件下，UPR可从促进存活转变为诱导细胞凋亡。AML细胞可操纵UPR途径以逃避凋亡，促进肿瘤进展并对抗各种治疗策略。本综述提供了关于AML中ER应激及其预后和治疗意义的当前知识。
