非酶糖基化形成的蛋白质高级糖基化终末产物（AGEs）可以破坏蛋白质的正常结构和功能，并刺激AGE受体（RAGE），引发与各种慢性疾病有关的复杂机制，包括胰腺癌。胰腺癌的许多常见风险因素是人体内蛋白质AGEs和糖基化应激的主要来源。蛋白AGEs的异常积累可以损害细胞蛋白组和促进AGE-RAGE驱动的促炎信号级联反应，导致氧化应激增加，蛋白酶抗性增加，蛋白质调控失调，STAT、NF-κB和AP-1的转录活性，泛素-蛋白酶体系统和自噬的异常状态，以及易感于癌变转化，向新生病变发展的其他分子事件。在本文中，我们回顾了一些研究，突出了我们对胰腺癌中蛋白质AGE形成和积累引发的受损蛋白组，失调功能网络和癌症特征间关联的分子事件的理解。

Protein advanced glycation end products (AGEs) formed by non-enzymatic glycation can disrupt the normal structure and function of proteins, and stimulate the receptor for AGEs (RAGE), triggering intricate mechanisms that are etiologically related to various chronic diseases, including pancreatic cancer. Many common risk factors of pancreatic cancer are the major sources for the formation of protein AGEs and glycative stress in the human body. Abnormal accumulation of protein AGEs can impair the cellular proteome and promote AGE-RAGE driven proinflammatory signaling cascades, leading to increased oxidative stress, protease resistance, protein dysregulation, transcription activity of STAT, NF-κB and AP-1, aberrant status in ubiquitin-proteasome system and autophagy, as well as other molecular events that are susceptible for the carcinogenic transformation towards the development of neoplasms. Here, we review studies to highlight our understanding in the orchestrated molecular events in bridging the impaired proteome, dysregulated functional networks, and cancer hallmarks initiated upon protein AGE formation and accumulation in pancreatic cancer.