摘要
肺动脉高压(PAH)是严重威胁人类健康的致命性疾病,其特点是肺血管阻力逐渐增高,最终导致右心衰竭和死亡。PAH的病理改变包括肺动脉的内皮功能障碍和血管重构。在这一过程中,基质金属蛋白酶(MMPs)及其组织抑制剂(TIMPs)之间的失衡起到了重要作用,尤其是在血管壁局部区域TIMPs过度表达而抑制MMPs活性,参与了内皮功能障碍的发生,并促进了细胞外基质过度沉积,最终导致血管重构。那么,如果减弱甚至抑制病变血管内TIMPs的过度表达会发生什么情况呢?由此,本文提出一个PAH治疗的新观点:对于已经发生严重重构的肺血管,减弱TIMPs的表达或许可以改善血管重构和血管内皮修复功能,最终有利于减轻甚至逆转重症PAH。
Pulmonary arterial hypertension （PAH） is a fatal disease threatening human health, which is characterized by a progressive increase in pulmonary vascular resistance, and ultimately lead to right heart failure and death. The pathological changes of PAH include endothelium dysfunction and vascular remodeling in pulmonary arteries. In the process of disease progres- sion, the imbalance between matrix metalloproteinases （MMPs） and tissue inhibitors of metalloproteinases （TIMPs） played an important role. The overexpression of TIMPs at local area of vessel wall inhibits the activity of MMPs, thus contribute to the occurrence of endothelium dysfunction, and promotes excessive accumulation of extracellular matrix （ ECM）, at last leads to vascular remodeling. Then, what would happen if the overexpression of TIMPs was weakened or inhibited in diseased pulmonary vessels？ This paper put forward a new idea for PAH treatment ： weakening TIMPs expression in pulmonary vessels where severe vascular remodeling exist, might reverse vascular remodeling and improve repair capabilities of vascular endothelium, at last benefit the recovery of PAH.
出处
《中国全科医学》
CAS
CSCD
北大核心
2013年第30期3526-3528,共3页
Chinese General Practice
基金
浙江省卫生高层次创新人才培养工程项目
关键词
高血压
肺性
内皮
血管
基质金属蛋白酶类
基质金属蛋白酶类组织抑制剂
治疗
Hypertension, pulmonary
Endothelium, vascular
Matrix metalloproteinases
Tissue inhibitor of metalloproteinases
Therapy
