Recent research has highlighted critical mechanisms underlying cardiovascular disease, particularly focusing on the role of various proteins and cellular interactions. For instance, the study by Ge et al. elucidates how MCT8 and OATP1C1 transport thyroid hormones across the blood-brain barrier, emphasizing their importance in neurological development and potential implications for cardiovascular health (ref: Ge doi.org/10.1016/j.cell.2025.06.032/). Kothari et al. further explore the immune response post-stroke, identifying the mast-cell-specific receptor Mrgprb2 as a regulator of inflammation, which could influence cardiovascular outcomes following ischemic events (ref: Kothari doi.org/10.1016/j.cell.2025.06.045/). Additionally, Krolak et al. demonstrate that endothelial gap junction coupling is essential for vasodilation during neurovascular coupling, suggesting that disruptions in this process may contribute to cardiovascular dysfunction (ref: Krolak doi.org/10.1016/j.cell.2025.06.030/). These studies collectively underscore the intricate interplay between neurovascular mechanisms and cardiovascular health, revealing potential therapeutic targets for intervention. Moreover, the impact of exercise on immune response and cancer treatment has been investigated by Phelps et al., who found that exercise enhances CD8 T cell antitumor immunity through microbiota metabolites, potentially linking physical activity to improved cardiovascular outcomes in cancer patients (ref: Phelps doi.org/10.1016/j.cell.2025.06.018/). Kaltenecker et al. delve into cancer cachexia, identifying hepatokines that promote wasting, which could indirectly affect cardiovascular health by altering metabolic states (ref: Kaltenecker doi.org/10.1016/j.cell.2025.06.039/). The integration of these findings highlights the multifaceted nature of cardiovascular disease mechanisms, suggesting that both metabolic and immune pathways are critical in understanding and addressing cardiovascular health.