Taherkhani Soroush, Sheibani Mohammad, Mohammadkhanizadeh Ali, Virag Jitka A I, de Castro Braz Lisandra, Azizi Yaser
Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Razi Drug Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Front Pharmacol. 2025 May 26;16:1559288. doi: 10.3389/fphar.2025.1559288. eCollection 2025.
Matrix metalloproteinases (MMPs) are a family of enzymes that play an important role in the pathophysiology of hypertensive disorders, particularly through their involvement in extracellular matrix (ECM) remodeling and vascular dysfunction. Their activity is closely linked to hypertension-mediated organ damage, which affects the vascular and cardio-renal systems. MMPs are responsible for degrading various components of the ECM, which is crucial for maintaining vascular structure and function. In hypertensive patients, several MMPs, including MMP-1, MMP-3, and MMP-9, are often found at elevated levels. This is associated with vascular remodeling and dysfunction due to chronic high blood pressure. The activation of MMPs in hypertension can be triggered by several factors, such as oxidative stress, inflammatory cytokines, and vasoactive agents like angiotensin II. In addition to increasing MMP activity, these variables cause an imbalance between MMPs and tissue inhibitors of metalloproteinases (TIMPs), which are the MMPs' natural inhibitors. This imbalance contributes to excessive degradation of the ECM and promotes pathological changes in vascular smooth muscle cells (VSMCs), leading to their transition from a contractile to a synthetic phenotype. This shift facilitates cell growth and migration, exacerbating vascular remodeling. Given their critical roles in hypertension-related organ damage, MMPs are being explored as potential pharmacological targets. Inhibitors of MMPs may help mitigate the adverse effects of hypertension by restoring balance in ECM remodeling processes. Understanding their mechanisms opens avenues for targeted therapies that could significantly improve outcomes for individuals suffering from hypertension-related complications.
基质金属蛋白酶(MMPs)是一类酶,在高血压疾病的病理生理学中发挥重要作用,特别是通过参与细胞外基质(ECM)重塑和血管功能障碍。它们的活性与高血压介导的器官损伤密切相关,这种损伤会影响血管和心肾系统。MMPs负责降解ECM的各种成分,这对维持血管结构和功能至关重要。在高血压患者中,经常发现几种MMPs水平升高,包括MMP-1、MMP-3和MMP-9。这与慢性高血压导致的血管重塑和功能障碍有关。高血压中MMPs的激活可由多种因素触发,如氧化应激、炎性细胞因子和血管活性物质如血管紧张素II。除了增加MMP活性外,这些变量还会导致MMPs与金属蛋白酶组织抑制剂(TIMPs)之间的失衡,TIMPs是MMPs的天然抑制剂。这种失衡导致ECM过度降解,并促进血管平滑肌细胞(VSMC)的病理变化,导致它们从收缩表型转变为合成表型。这种转变促进细胞生长和迁移,加剧血管重塑。鉴于它们在高血压相关器官损伤中的关键作用,MMPs正被探索为潜在的药理学靶点。MMPs抑制剂可能有助于通过恢复ECM重塑过程中的平衡来减轻高血压的不良影响。了解它们的机制为靶向治疗开辟了途径,这可能显著改善患有高血压相关并发症个体的预后。