Endothelial senescence of the vertebral artery in the context of cervical degeneration: biomechanically driven remodeling of the hemodynamic environment.

Cervical spine degeneration is frequently accompanied by long-term alterations in the hemodynamic environment of the vertebral arteries. Traditionally, vascular abnormalities associated with cervical degeneration have been interpreted mainly from the perspectives of structural compression or macroscopic hemodynamic disturbance. However, these explanations do not fully account for the functional instability of posterior circulation perfusion that may occur even in the absence of overt arterial stenosis. Emerging evidence suggests that endothelial senescence represents a central biological process linking chronic mechanical stress, disturbed flow patterns, and progressive vascular dysfunction. In the vertebral artery, which is anatomically coupled to the cervical spine and exposed to dynamic biomechanical forces, long-term alterations in vascular geometry and shear stress may gradually reshape the local microenvironment of the vascular wall. These changes can promote endothelial stress responses, metabolic imbalance, and inflammatory signaling, ultimately facilitating the development of endothelial senescence.In this review, we integrate current knowledge from vascular biology, mechanobiology, and cerebrovascular physiology to examine how cervical degenerative changes may remodel the vertebral artery microenvironment. We discuss the molecular basis of endothelial senescence, the role of disturbed flow in activating pro-senescent signaling pathways, and the potential consequences of endothelial aging for the functional stability of the posterior circulation. By framing vertebral artery-related abnormalities within the context of endothelial senescence and vascular microenvironment remodeling, this perspective provides a conceptual framework that may help explain chronic posterior circulation vulnerability associated with cervical degeneration and identify potential directions for future mechanistic and translational research.