Hantaviruses are zoonotic RNA viruses that cause a spectrum of diseases, including hemorrhagic fever with renal syndrome and hantavirus cardiopulmonary syndrome. Although clinical manifestations vary among hantavirus species, increasing evidence suggests that disease severity is driven primarily by dysregulated host immune responses and vascular dysfunction rather than direct viral cytopathic effects alone. Hantaviruses exhibit a marked tropism for endothelial and immune cells, where infection alters inflammatory signaling pathways and disrupts vascular homeostasis. Increased endothelial permeability and capillary leakage are central features of severe disease and are associated with cytokine amplification, leukocyte recruitment, and endothelial barrier dysregulation. Multiple mediators, including tumor necrosis factor-α, interleukin-6, interferon-γ, vascular endothelial growth factor, and bradykinin-related pathways, have been implicated in the pathogenesis of tissue edema and vascular instability. Current evidence further suggests that endothelial injury in hantavirus infection is predominantly functional rather than structurally destructive, reflecting complex interactions between viral persistence, host inflammatory responses, and vascular signaling networks. This review summarizes current understanding of the molecular and immunopathogenic mechanisms underlying hantavirus-associated vascular disease, with particular emphasis on endothelial dysregulation, cytokine-mediated injury, and permeability signaling pathways.