细胞外囊泡在铁稳态和铁下垂中的作用:聚焦于肌肉骨骼疾病。

IF 3.6 3区生物学 Q3 CELL BIOLOGY

Traffic Pub Date : 2023-09-01 DOI:10.1111/tra.12905

Zhiwei Liao, Bide Tong, Zixuan Ou, Junyu Wei, Ming Lei, Cao Yang

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引用次数: 0

摘要

铁稳态对维持正常的细胞功能至关重要，其破坏被认为是肌肉骨骼疾病的致病机制之一。在氧化应激条件下，细胞铁超载和脂质过氧化的积累可导致铁下垂。细胞外囊泡(Extracellular vesicles, ev)作为细胞间通讯的介质，在调节细胞铁凋亡的结果中发挥重要作用。越来越多的证据表明，EV的生物发生和分泌与细胞铁输出密切相关。此外，不同来源的ev提供不同的货物，在受体细胞中引起表型变化，激活或抑制铁下垂。因此，通过ev提供针对铁下垂的治疗可能具有治疗肌肉骨骼疾病的巨大潜力。本文旨在综述ev在铁稳态和铁凋亡中的作用，以及它们在肌肉骨骼疾病中的治疗应用，从而为研究和临床实践提供有价值的见解。

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The role of extracellular vesicles in iron homeostasis and ferroptosis: Focus on musculoskeletal diseases.

Iron homeostasis is crucial for maintaining proper cellular function, and its disruption is considered one of the pathogenic mechanisms underlying musculoskeletal diseases. Under conditions of oxidative stress, the accumulation of cellular iron overload and lipid peroxidation can lead to ferroptosis. Extracellular vesicles (EVs), serving as mediators in the cell‐to‐cell communication, play an important role in regulating the outcome of cell ferroptosis. Growing evidence has proven that EV biogenesis and secretion are tightly associated with cellular iron export. Furthermore, different sources of EVs deliver diverse cargoes to bring about phenotypic changes in the recipient cells, either activating or inhibiting ferroptosis. Thus, delivering therapies targeting ferroptosis through EVs may hold significant potential for treating musculoskeletal diseases. This review aims to summarize current knowledge on the role of EVs in iron homeostasis and ferroptosis, as well as their therapeutic applications in musculoskeletal diseases, and thereby provide valuable insights for both research and clinical practice.

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来源期刊

Traffic 生物-细胞生物学

CiteScore

8.10

自引率

2.20%

发文量

审稿时长

2 months

期刊介绍： Traffic encourages and facilitates the publication of papers in any field relating to intracellular transport in health and disease. Traffic papers span disciplines such as developmental biology, neuroscience, innate and adaptive immunity, epithelial cell biology, intracellular pathogens and host-pathogen interactions, among others using any eukaryotic model system. Areas of particular interest include protein, nucleic acid and lipid traffic, molecular motors, intracellular pathogens, intracellular proteolysis, nuclear import and export, cytokinesis and the cell cycle, the interface between signaling and trafficking or localization, protein translocation, the cell biology of adaptive an innate immunity, organelle biogenesis, metabolism, cell polarity and organization, and organelle movement. All aspects of the structural, molecular biology, biochemistry, genetics, morphology, intracellular signaling and relationship to hereditary or infectious diseases will be covered. Manuscripts must provide a clear conceptual or mechanistic advance. The editors will reject papers that require major changes, including addition of significant experimental data or other significant revision. Traffic will consider manuscripts of any length, but encourages authors to limit their papers to 16 typeset pages or less.