Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
School of Medicine, Keele University, Keele, UK.
J Cell Physiol. 2023 Jun;238(6):1148-1159. doi: 10.1002/jcp.31019. Epub 2023 Apr 11.
Hypertension remains a major contributor to cardiovascular disease (CVD), a leading cause of global death. One of the major insults that drive increased blood pressure is inflammation. While it is the body's defensive response against some homeostatic imbalances, inflammation, when dysregulated, can be very deleterious. In this review, we highlight and discuss the causative relationship between inflammation and hypertension. We critically discuss how the interplay between inflammation and reactive oxygen species evokes endothelial damage and dysfunction, ultimately leading to narrowing and stiffness of blood vessels. This, along with phenotypic switching of the vascular smooth muscle cells and the abnormal increase in extracellular matrix deposition further exacerbates arterial stiffness and noncompliance. We also discuss how hyperhomocysteinemia and microRNA act as links between inflammation and hypertension. The premises we discuss suggest that the blue-sky scenarios for targeting the underlying mechanisms of hypertension necessitate further research.
高血压仍然是心血管疾病(CVD)的主要诱因,也是全球死亡的主要原因之一。导致血压升高的主要损伤之一是炎症。虽然炎症是身体对某些体内平衡失衡的防御反应,但当炎症失调时,可能会非常有害。在这篇综述中,我们强调并讨论了炎症与高血压之间的因果关系。我们批判性地讨论了炎症和活性氧之间的相互作用如何引起内皮损伤和功能障碍,最终导致血管狭窄和僵硬。此外,血管平滑肌细胞的表型转换和细胞外基质沉积的异常增加进一步加剧了动脉僵硬和顺应性降低。我们还讨论了高同型半胱氨酸血症和 microRNA 如何作为炎症和高血压之间的联系。我们讨论的前提表明,针对高血压潜在机制的蓝天方案需要进一步研究。