Department of Biochemistry, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania.
Int J Mol Sci. 2024 Aug 14;25(16):8838. doi: 10.3390/ijms25168838.
Type 2 diabetes (T2D) and Parkinson's disease (PD) are the two most frequent age-related chronic diseases. There are many similarities between the two diseases: both are chronic diseases; both are the result of a decrease in a specific substance-insulin in T2D and dopamine in PD; and both are caused by the destruction of specific cells-beta pancreatic cells in T2D and dopaminergic neurons in PD. Recent epidemiological and experimental studies have found that there are common underlying mechanisms in the pathophysiology of T2D and PD: chronic inflammation, mitochondrial dysfunction, impaired protein handling and ferroptosis. Epidemiological research has indicated that there is a higher risk of PD in individuals with T2D. Moreover, clinical studies have observed that the symptoms of Parkinson's disease worsen significantly after the onset of T2D. This article provides an up-to-date review on the intricate interplay between oxidative stress, reactive oxygen species (ROS) and ferroptosis in PD and T2D. By understanding the shared molecular pathways and how they can be modulated, we can develop more effective therapies, or we can repurpose existing drugs to improve patient outcomes in both disorders.
2 型糖尿病（T2D）和帕金森病（PD）是两种最常见的与年龄相关的慢性疾病。这两种疾病有许多相似之处：都是慢性疾病；都是由于特定物质减少引起的，T2D 是胰岛素，PD 是多巴胺；都是由特定细胞破坏引起的，T2D 是β胰岛细胞，PD 是多巴胺能神经元。最近的流行病学和实验研究发现，T2D 和 PD 的病理生理学存在共同的潜在机制：慢性炎症、线粒体功能障碍、蛋白质处理受损和铁死亡。流行病学研究表明，T2D 患者患 PD 的风险更高。此外，临床研究观察到 T2D 发病后帕金森病的症状明显恶化。本文对 PD 和 T2D 中氧化应激、活性氧（ROS）和铁死亡之间的复杂相互作用进行了最新综述。通过了解共同的分子途径以及如何调节这些途径，我们可以开发更有效的治疗方法，或者我们可以重新利用现有的药物来改善两种疾病患者的预后。
