The right ventricle (RV) differs developmentally, anatomically and functionally from the left ventricle (LV). Therefore, characteristics of LV adaptation to chronic pressure overload cannot easily be extrapolated to the RV. Mitochondrial abnormalities are considered a crucial contributor in heart failure (HF), but have never been compared directly between RV and LV tissues and cardiomyocytes. To identify ventricle-specific mitochondrial molecular and functional signatures, we established rat models with two slowly developing disease stages (compensated and decompensated) in response to pulmonary artery banding (PAB) or ascending aortic banding (AOB). Genome-wide transcriptomic and proteomic analyses were used to identify differentially expressed mitochondrial genes and proteins and were accompanied by a detailed characterization of mitochondrial function and morphology. Two clearly distinguishable disease stages, which culminated in a comparable systolic impairment of the respective ventricle, were observed. Mitochondrial respiration was similarly impaired at the decompensated stage, while respiratory chain activity or mitochondrial biogenesis were more severely deteriorated in the failing LV. Bioinformatics analyses of the RNA-seq. and proteomic data sets identified specifically deregulated mitochondrial components and pathways. Although the top regulated mitochondrial genes and proteins differed between the RV and LV, the overall changes in tissue and cardiomyocyte gene expression were highly similar. In conclusion, mitochondrial dysfuntion contributes to disease progression in right and left heart failure. Ventricle-specific differences in mitochondrial gene and protein expression are mostly related to the extent of observed changes, suggesting that despite developmental, anatomical and functional differences mitochondrial adaptations to chronic pressure overload are comparable in both ventricles.

右心室 (RV) 在发育、解剖学和功能上与左心室 (LV) 不同。因此，左心室对慢性压力超负荷的适应特征不能轻易外推到右心室。线粒体异常被认为是心力衰竭 (HF) 的关键因素，但从未在 RV 和 LV 组织以及心肌细胞之间进行直接比较。为了识别心室特异性线粒体分子和功能特征，我们建立了具有两个缓慢发展的疾病阶段（代偿期和失代偿期）的大鼠模型，以响应肺动脉束带（PAB）或升主动脉束带（AOB）。全基因组转录组和蛋白质组分析用于鉴定差异表达的线粒体基因和蛋白质，并伴有线粒体功能和形态的详细表征。观察到两个明显可区分的疾病阶段，最终导致相应心室的可比收缩损害。线粒体呼吸在失代偿阶段同样受到损害，而呼吸链活性或线粒体生物发生在衰竭的左心室中恶化得更严重。 RNA-seq 的生物信息学分析。蛋白质组数据集明确了线粒体成分和途径的失调。尽管右心室和左心室之间最受调控的线粒体基因和蛋白质不同，但组织和心肌细胞基因表达的总体变化高度相似。总之，线粒体功能障碍导致右心衰竭和左心衰竭的疾病进展。线粒体基因和蛋白质表达的心室特异性差异主要与观察到的变化程度有关，这表明尽管发育、解剖和功能存在差异，但两个心室的线粒体对慢性压力超负荷的适应是相当的。