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阿尔茨海默病中靶向铁死亡的机制、生物学及作用的研究进展:最新综述

Insights into targeted ferroptosis in mechanisms, biology, and role of Alzheimer's disease: an update.

作者信息

Zhou Bingyuan, Li Jing, Wu Anqi, Wang Xuewei, Cheng Le, Yang Gaoshang, Gao Dahong, Zhu Caifeng

机构信息

The First Clinical Medical School, Anhui University of Traditional Chinese Medicine, Hefei, China.

Fourth Department of Encephalopathy, Second Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei, Anhui, China.

出版信息

Front Aging Neurosci. 2025 Jul 21;17:1587986. doi: 10.3389/fnagi.2025.1587986. eCollection 2025.

Abstract

Ferroptosis is a newly discovered form of programmed cell death, primarily caused by an imbalance between iron-dependent oxidative damage and antioxidant defense mechanisms within the cell. It differs from previously reported forms of cell death, such as apoptosis, necrosis, and autophagy, in terms of morphology, biochemistry, and genetics. Alzheimer's disease (AD) is the most common neurodegenerative disorder, characterized by pathological features including neurofibrillary tangles (NFTs), senile plaques (SPs), and abnormal iron deposition, suggesting that ferroptosis may be involved in its disease progression. Although recent studies have made significant progress, the mechanisms underlying neuronal ferroptosis in AD remain incompletely understood. This review, based on elucidating the process and regulatory mechanisms of cellular ferroptosis, explores, and supplements the correlation between iron overload and redox imbalance with the main pathological mechanisms of AD, providing new insights for the treatment of AD and the development of new drugs.

摘要

铁死亡是一种新发现的程序性细胞死亡形式,主要由细胞内铁依赖性氧化损伤与抗氧化防御机制之间的失衡引起。在形态学、生物化学和遗传学方面,它不同于先前报道的细胞死亡形式,如凋亡、坏死和自噬。阿尔茨海默病(AD)是最常见的神经退行性疾病,其病理特征包括神经原纤维缠结(NFTs)、老年斑(SPs)和异常铁沉积,这表明铁死亡可能参与其疾病进展。尽管最近的研究取得了重大进展,但AD中神经元铁死亡的潜在机制仍未完全了解。本综述在阐明细胞铁死亡过程和调控机制的基础上,探讨并补充了铁过载和氧化还原失衡与AD主要病理机制之间的相关性,为AD的治疗和新药研发提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/faf0/12319056/900cfd896c6a/fnagi-17-1587986-g0001.jpg

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