活性氧引起缺氧诱导因子1活化参与肺动脉高压血管重塑的分子机制

Molecular Mechanism of Hypoxia-inducible Factor-1 Activation Induced by Reactive Oxygen Species in Vascular Remodeling of Pulmonary Hypertension

肺动脉高压的特点是血管收缩和血管平滑肌细胞增生,导致肺动脉血管的病理性重塑.活性氧介导缺氧诱导因子1的活化,通过一系列的下游细胞信号,引起肺血管的异常调节,造成管壁肥大和增厚,在肺动脉高压的血管重塑中起关键作用.肺动脉高压时,针对活性氧和缺氧诱导因子1的干预,以调节氧化还原信号为中心的治疗方法,有望成为本病治疗新的策略和重要靶点,现就此做一详细阐述.

Pulmonary hypertension(PH)is characterized by vasoconstriction and proliferation of vascular smooth muscle cells,leading to pathological remodeling of pulmonary arteries.ROS mediates the activation of hypoxia-inducible factor-1(HIF-1).Through a series of downstream cell signals,it causes abnormal regulation of pulmonary vessels,resulting in hypertrophy and thickening of the vessel wall,which plays a key role in the vascular remodeling of PH.For the intervention of ROS and HIF-1 in PH,the treatment method centering on the regulation of redox signal is expected to become a new strategy and an important target for the treatment of this disease.This paper will elaborate on these in detail.