Right-sided heart failure is a common consequence of pulmonary arterial hypertension. Overloading the right ventricle results in hypertrophy, which progresses to failure characterised by impaired Ca²⁺ dynamics and force production that is linked with transverse(t)-tubule remodelling. This also unloads the left ventricle, which consequently atrophies. Experimental left‑ventricular unloading can result in t-tubule remodelling, but it is currently unclear if this occurs in right-sided heart failure. In this work, we studied the monocrotaline (MCT)-induced right heart failure in the rat, using confocal microscopy to investigate cellular remodelling of t-tubules, junctophilin-2 (JPH2), and ryanodine receptor-2 (RyR2). We examined remodelling across tissue anatomical regions of both ventricles: trabeculae, papillary muscles, and free walls. Our analyses demonstrated in MCT hearts significant loss of t-tubule periodicity, disruption of the normal sarcomere striated pattern with JPH2 labelling, and also a disorganised striated pattern of RyR2 - a feature not previously reported in heart failure. Remodelling of JPH2 and RyR2 in the MCT heart was more pronounced in papillary muscles and trabeculae - particularly in the left ventricle, indicating that these anatomical structures, used as ex vivo isolated muscle preparations, are more sensitive to the disease process.

中文翻译：

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右心衰竭患者萎缩左心室横小管重构

右侧心力衰竭是肺动脉高压的常见后果。右心室超负荷导致肥大，进而发展为以 Ca ²⁺受损为特征的衰竭与横向（t）-小管重塑相关的动力学和力产生。这也会减轻左心室的负荷，从而导致萎缩。实验性左心室减负荷可导致 t 小管重构，但目前尚不清楚这是否发生在右侧心力衰竭中。在这项工作中，我们研究了野百合碱 (MCT) 诱导的大鼠右心衰竭，使用共聚焦显微镜研究了 t 小管、junctophilin-2 (JPH2) 和兰尼碱受体-2 (RyR2) 的细胞重塑。我们检查了两个心室组织解剖区域的重塑：小梁、乳头肌和游离壁。我们的分析表明，在 MCT 心脏中，t 小管周期性显着丧失，用 JPH2 标记破坏了正常的肌节条纹模式，还有一种杂乱无章的 RyR2 条纹模式——以前在心力衰竭中没有报道过这种特征。MCT 心脏中 JPH2 和 RyR2 的重构在乳头肌和小梁中更为明显 - 特别是在左心室，表明这些解剖结构用作离体分离的肌肉制剂，对疾病过程更敏感。