Vascular Aging Produces Vulnerability to Ischemic Stroke
Ischemic stroke is an age-related condition, in which atherosclerotic plaque ruptures to block blood supply to a part of the brain for long enough to cause dysfunction, reperfusion injury, and cell death. If the harmed region of the brain is critical, the patient dies. Otherwise, the result is a lasting loss of function. Even given the brain's plasticity, that loss may never be fully restored. The aging of the vasculature is evidently critical to both the occurrence and severity of stroke. Researchers here review this topic and the mechanisms thought important in determining risk and severity of stroke.
In recent years, the intricate pathogenesis and potential interventions for ischemic stroke (IS) have been an intriguing area of research. Although there are some feasible treatments for IS, more effective treatments are still urgently needed. More and more evidence has indicated the vital roles of vascular aging in the pathology of IS with the involvement of oxidative stress and inflammatory response. Therefore, the identification of novel targets and the development of effective interventions that can modulate vascular aging by regulating oxidative stress and inflammatory response are worth continued research efforts. Only by unraveling the intricate pathogenesis and exploring more accurate targets can light be shed on how the risk of IS can be mitigated and the patient's quality of life improved with the innovation of more effective therapies.
Vascular aging is critically involved in the pathology of IS. Cellular senescence refers to a stress-induced, permanent cessation of the cell cycle, which leads to adverse functional and structural changes. Increased senescent cells in blood vessels tend to induce vascular aging within aging organisms, which brings about a gradual deterioration in oxidative stress and inflammatory response. This deterioration usually results in endothelial dysfunction and vascular remodeling, which increases the susceptibility and exacerbates the pathology of IS. Further uncovering the underlying mechanisms of vascular aging and IS holds significant implications for advancing our understanding and therapeutic strategies. In this review, we conclude that vascular aging is a multifaceted contributor to IS. It promotes endothelial dysfunction and drives vascular remodeling, which is marked by both oxidative stress and inflammatory response. These interconnected factors collectively amplify the susceptibility and pathological severity of IS.