Crosstalk between Oxidative Stress and Exosomes

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Mammals have several organs comprising various cells with different functions. Furthermore, eukaryotic cells are compartmentalized into functionally distinct organelles. Thus, for good organismal health, exosomes, which play an important role in cell-to-cell communication, interact closely with oxidative stress. Oxidative stress, which is recognized as a type of intracellular second signal, is aggravated by reactive species. As a subtype of reactive species, reactive oxygen species (ROS) can be produced on the extracellular face of the plasma membrane by NADPH oxidases, via the mitochondrial electron transport chain, in peroxisomes, and in the lumen of the endoplasmic reticulum. The scavenging of ROS is mainly dependent on peroxiredoxins, including GSH peroxidases, peroxiredoxins 3 and 5, and thioredoxin reductase. Intracellular ROS increase the number of intracellular multivesicular bodies (MVBs) by restraining their degradation in lysosomes, thereby enhancing the release of exosomes under the synergy of the depletion of exofacial GSH, which can be regulated by oxidative stress. In contrast, higher ROS levels can decrease the yield of exosomes by activating cellular autophagy to degrade MVBs. Moreover, exosomes can transfer the characteristics of parent cells to recipient cells. Here, we review the interaction between oxidative stress and exosomes in the hope of providing insi

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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