Extracellular vesicles in health, aging and disease (IMAGE)
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Figure 1. Stress-induced EV release by normal, stressed, aging, and cancer cells and their associated molecular cargo. Each EV type carries molecular cargo depending on the stressor and cell of origin. Senescence increases SA-EV output enriched with chromosomal DNA fragments and EphA2, promoting proliferation in Ephril-A1-positive cells via ceramide-dependent biogenesis [51]. Oxidative stress elevates intracellular Ca2+ and ROS, triggering microvesicle shedding and exosomes carrying mtDNA, oxidized proteins, and stress chaperones [15]. Hypoxia enhances exosome release with HIF-1a-driven cargo such as miR-210 and VEGF to promote angiogenesis [52]. Ionizing radiation activates p54 and TSAP6, producing EVs carrying altered miRNAs and gH2AX that induce bystander DNA-damage responses [53]. Apoptosis generates large ApoEVs containing DNA, histones, organelles, and cytosolic proteins, affecting immunity and tissue remodeling [54]. Chemotherapy and ER stress remodel EV cargo, including P-gp and PD-L1, promoting drug resistance and immune evasion [55].
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Copyright: © 2026 Umeris et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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