Division of Pulmonary, Critical Care, Sleep and Occupational Medicine, Department of Medicine, Indiana University School of Medicine , Indianapolis, Indiana.
Pulmonary Hypertension Research Group, Institut Universitaire de Cardiologie et de Pneumologie de Québec Research Center, Laval University , Quebec City, Quebec , Canada.
Am J Physiol Lung Cell Mol Physiol. 2018 Mar 1;314(3):L443-L460. doi: 10.1152/ajplung.00374.2017. Epub 2017 Nov 2.
Right ventricular (RV) function is the primary prognostic factor for both morbidity and mortality in pulmonary hypertension (PH). RV hypertrophy is initially an adaptive physiological response to increased overload; however, with persistent and/or progressive afterload increase, this response frequently transitions to more pathological maladaptive remodeling. The mechanisms and disease processes underlying this transition are mostly unknown. Angiogenesis has recently emerged as a major modifier of RV adaptation in the setting of pressure overload. A novel paradigm has emerged that suggests that angiogenesis and angiogenic signaling are required for RV adaptation to afterload increases and that impaired and/or insufficient angiogenesis is a major driver of RV decompensation. Here, we summarize our current understanding of the concepts of maladaptive and adaptive RV remodeling, discuss the current literature on angiogenesis in the adapted and failing RV, and identify potential therapeutic approaches targeting angiogenesis in RV failure.
右心室（RV）功能是肺动脉高压（PH）患者发病率和死亡率的主要预测因素。RV 肥厚最初是对负荷增加的适应性生理反应；然而，随着后负荷持续和/或进行性增加，这种反应常常转变为更具病理性的适应性重构不良。导致这种转变的机制和疾病过程大部分尚不清楚。血管生成最近已成为压力超负荷情况下 RV 适应性的主要调节因素。一个新的范式已经出现，即血管生成和血管生成信号对于 RV 适应后负荷增加是必需的，而血管生成受损和/或不足是 RV 失代偿的主要驱动因素。在这里，我们总结了我们目前对适应性和适应性 RV 重构不良概念的理解，讨论了适应性和衰竭 RV 中血管生成的当前文献，并确定了针对 RV 衰竭中血管生成的潜在治疗方法。
