目前肺动脉高压（PAH）治疗主要聚焦在肺血管病变，针对右心室的研究还处于探索阶段。适应性和难适应性右心室重构中普遍存在心肌缺血和毛细血管稀疏引起的心肌需氧量增加，需要通过激活一些转录因子来适应低氧环境。右心室对PAH适应有很大可变性，但确切机制尚未阐明。前期研究中我们发现难适应性右心室重构中线粒体能量代谢完全转变为糖酵解，改善线粒体功能可延缓右心室衰竭进展。因此，我们推测线粒体代谢损伤是右心室肥厚向右心室衰竭进展的关键原因之一。为证实这一假说，我们拟使用两种适应性和难适应性右心室重构模型，采用分子生物学等技术，从心肌缺血/毛细血管缺失-线粒体代谢损伤-糖酵解增强三个层次，观察线粒体代谢从适应性向难适应性右心室重构转变过程中的作用，明确提高葡萄糖氧化有助于"心肌冬眠"复苏和右心室重构改善。本研究是PAH病理生物学新兴内容，整合能量代谢理论方法与现有治疗目标是未来右心衰竭治疗策略之一。

Most pulmonary arterial hypertension (PAH) therapies focus on regressing pulmonary vascular disease, the cause of right ventricular failure is unclear and understudies. Myocardial ischemia and the arteriolar-capillary rarefaction are more common in both maladaptive and adaptive right ventricular remodeling, which enhanced myocardial O2 consumption as well as activated transcription factors to hypoxia condition. However, there remains a significant variability in right ventricular adaptation to PAH. In our previous studies, we found that the energy metabolic shift from oxidative mitochondrial metabolism to the less energy efficient glycolytic metabolism may reflect maladaptive right ventricular remodeling, this suggested that improving mitochondrial function might be therapeutic. Therefore, we hypothesize that mitochondrial impair was the leading cause from right ventricular hypertrophy to failure. We try to establish two adaptive and maladaptive right ventricular remodeling models, using molecular biotechnology, analyzed the effects of mitochondrial metabolism on right ventricular remodeling from adaptive to maladaptive by ischemia/arteriolar-capillary rarefaction-mitochondrial impair-increased glycolysis. This may help us to understand increased glucose oxidation has been beneficial for resuscitating hibernation and improving right ventricular remodeling. As the emerging concepts of right heart pathobiology in PAH, integrate energy metabolic theoretical method and therapeutic goals may offer selective strategies for improving right heart failure.