Extracellular vesicles (EVs) are emerging as pivotal players in cancer therapy, particularly in the development of personalized cancer vaccines. One innovative approach involves engineering pyroptotic vesicles, which are derived from tumor cell pyroptosis, to create a personalized vaccine platform that can effectively stimulate the immune system against tumors (ref: Li doi.org/10.1038/s41565-025-01931-2/). Another study introduced microwave-assisted methods for preparing tumor-derived microparticles (TMPs), which demonstrated enhanced immunogenicity compared to traditional UV-derived TMPs, indicating a promising avenue for tumor immunotherapies (ref: Wu doi.org/10.1038/s41565-025-01922-3/). Furthermore, the role of exosomes in promoting colorectal cancer liver metastasis was highlighted, showing that high liver GP73 expression correlates with increased exosome-dependent metastasis, suggesting a potential target for therapeutic intervention (ref: Huang doi.org/10.1186/s12943-025-02350-6/). Additionally, LMTK3 was identified as a regulator of EV biogenesis, influencing tumor growth by modulating the immune microenvironment, thus presenting another layer of complexity in cancer therapy (ref: Samuels doi.org/10.1186/s12943-025-02346-2/). The development of novel diagnostic tools, such as a nanohole array for high-throughput counting of single EVs, further underscores the potential of EVs in non-invasive cancer screening (ref: Yin doi.org/10.1002/anie.202506744/). Lastly, psychological stress was shown to promote pancreatic cancer progression via RNA transfer through EVs, linking stress responses to cancer biology (ref: Chen doi.org/10.1038/s41556-025-01667-0/).

The role of extracellular vesicles (EVs) in immune regulation is multifaceted, with studies revealing their influence on various immune responses. LMTK3's regulation of EV biogenesis was shown to promote tumor growth by reducing monocyte infiltration and driving pro-tumorigenic macrophage polarization in breast cancer, highlighting the interplay between EVs and the immune microenvironment (ref: Samuels doi.org/10.1186/s12943-025-02346-2/). Psychological stress was also implicated in immune modulation, as it was found to induce ALKBH5 deficiency, promoting tumor innervation and pancreatic cancer progression through EV-mediated RNA transfer (ref: Chen doi.org/10.1038/s41556-025-01667-0/). Furthermore, the optimization of EV labeling techniques was addressed, revealing that non-specific particle formation during labeling can confound results, thus emphasizing the need for reproducible methods in EV research (ref: Haines doi.org/10.1002/jev2.70079/). The development of nano-flow cytometry for the discrimination and separation of viral particles and EVs also represents a significant advancement in understanding EV dynamics in infectious contexts (ref: Bokun doi.org/10.1002/jev2.70060/). Additionally, erythrocyte-derived EVs were shown to play a role in maintaining homeostasis within the integumentary system, suggesting a broader impact of EVs on physiological processes (ref: Cao doi.org/10.1002/jev2.70080/).

Understanding the mechanisms of extracellular vesicle (EV) biogenesis and function is crucial for harnessing their therapeutic potential. LMTK3 was identified as a key regulator of EV biogenesis, affecting cargo sorting and promoting tumor growth by altering the immune landscape in breast cancer (ref: Samuels doi.org/10.1186/s12943-025-02346-2/). The study of GP73 also revealed its role in exosome biogenesis, where high expression levels correlated with increased colorectal cancer liver metastasis, indicating that targeting these pathways could be beneficial in cancer treatment (ref: Huang doi.org/10.1186/s12943-025-02350-6/). Additionally, the impact of psychological stress on EV-mediated RNA transfer in pancreatic cancer progression was explored, suggesting that stress responses can significantly influence tumor biology (ref: Chen doi.org/10.1038/s41556-025-01667-0/). The optimization of EV labeling techniques was highlighted as essential for accurate EV research, addressing the challenges of non-specific particle formation during labeling (ref: Haines doi.org/10.1002/jev2.70079/). Furthermore, the regulation of ectosome formation in B lymphocytes by CD24 was elucidated, showcasing the intricate signaling pathways involved in EV biogenesis (ref: Phan doi.org/10.1002/jev2.70093/).

Extracellular vesicles (EVs) are increasingly recognized for their roles in neurological disorders, particularly in the context of Alzheimer's disease (AD) and Parkinson's disease (PD). Research has shown that gut microbiota-derived EVs can influence neuroinflammatory processes along the gut-brain axis, potentially impacting the onset and progression of AD (ref: Xie doi.org/10.1080/19490976.2025.2501193/). In the realm of PD, EVs derived from patients were analyzed for their suitability as therapeutic vehicles, revealing that they could effectively deliver shRNA minicircles to prevent parkinsonian pathology (ref: Izco doi.org/10.1186/s40035-025-00484-7/). Additionally, the optimization of EV labeling techniques was addressed, highlighting the importance of reproducible methods in studying EV dynamics in neurological contexts (ref: Haines doi.org/10.1002/jev2.70079/). The relationship between erythrocyte-derived EVs and the integumentary system was also explored, suggesting that these vesicles play a role in maintaining homeostasis, which could have implications for neurological health (ref: Cao doi.org/10.1002/jev2.70080/).

The role of extracellular vesicles (EVs) in metabolic disorders has garnered attention, particularly regarding their impact on inflammation and cellular dysfunction. A study demonstrated that lipotoxic hepatocyte-derived EVs induce inflammation in the liver and pancreas, leading to beta cell dysfunction, with macrophage TLR4 playing a crucial role in this process (ref: Alén doi.org/10.1007/s00125-025-06445-z/). This highlights the potential of targeting EV-mediated pathways to mitigate metabolic complications. Additionally, the development of 3D-printed titanium scaffolds loaded with exosomes for bone regeneration illustrates the innovative applications of EVs in regenerative medicine (ref: Luo doi.org/10.1002/advs.202500599/). Furthermore, research on myelin reduction in patients with monogenic small vessel disease suggests that EVs may be involved in the cognitive impairments associated with this condition, linking EV dynamics to neurological outcomes (ref: Denecke doi.org/10.1002/alz.70127/).

Extracellular vesicles (EVs) play a significant role in cardiovascular health, with emerging research linking them to various cardiovascular conditions. A genome-wide association study of long COVID revealed potential mechanisms underlying persistent symptoms, including cardiovascular manifestations, highlighting the need for further investigation into the role of EVs in post-viral syndromes (ref: Lammi doi.org/10.1038/s41588-025-02100-w/). Additionally, the impact of chemotherapy-free neoadjuvant therapies on HER2-enriched early breast cancer was explored, with implications for cardiovascular health in cancer patients (ref: Kuemmel doi.org/10.1016/S1470-2045(25)00097-X/). The loss of lipid asymmetry in plasma membranes, which facilitates membrane blebbing and EV formation, was also investigated, suggesting that alterations in EV dynamics could influence cardiovascular health (ref: Wang doi.org/10.1073/pnas.2417145122/).

Extracellular vesicles (EVs) are increasingly recognized for their roles in infectious diseases, particularly in the context of viral infections. A study on Enterovirus D68 (EV-D68) characterized its epidemiology and clinical severity among children, emphasizing the need for improved surveillance and understanding of EV dynamics in respiratory illnesses (ref: Clopper doi.org/10.1001/jamanetworkopen.2025.9131/). Additionally, the loss of lipid asymmetry in plasma membranes, which facilitates EV formation, was linked to membrane blebbing and intercellular communication, suggesting that EVs may play a role in the pathophysiology of infectious diseases (ref: Wang doi.org/10.1073/pnas.2417145122/). The exploration of gene expression reprogramming in 'hibernating' cells further underscores the complex interactions between EVs and cellular responses to stressors, which could have implications for infectious disease management (ref: Engelfriet doi.org/10.7554/eLife.101186/).