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肺动脉高压引起的肺动脉异常重构是由多种途径导致的,微小核糖核酸、钾离子通道及生存素等在其中发挥重要作用,它们抑制了平滑肌细胞及内皮细胞的凋亡,使肺血管中膜增厚和重构导致了肺动脉的不可逆变化,最终引起肺动脉压力的持续增高。明确肺动脉异常重构发生的分子机制,寻找能够延缓或逆转此病理过程的有效生物学方法,成为科学领域进一步探索研究的热点。
Pulmonary hypertension caused by abnormal pulmonary remodeling is caused by a variety of ways, microRNA, potassium channels and survivin play an important role in them, they inhibit the smooth muscle cells and endothelial cell apoptosis, the pulmonary vascular membrane Thickening and remodeling lead to irreversible changes in pulmonary arteries, which eventually cause a sustained increase in pulmonary artery pressure. To clarify the molecular mechanism of abnormal pulmonary remodeling and to find effective biological methods that can delay or reverse this pathological process has become a hot spot for further exploration in the field of science.