Adverse cardiac remodelling clinically manifests as deleterious changes to heart architecture (size, mass and geometry) and function. These changes, which include alterations to ventricular wall thickness, chamber dilation and poor contractility, are important because they progressively drive patients with cardiac disease towards heart failure and are associated with poor prognosis. Cysteine cathepsins contribute to key signalling pathways involved in adverse cardiac remodelling including synthesis and degradation of the cardiac extracellular matrix (ECM), cardiomyocyte hypertrophy, impaired cardiomyocyte contractility and apoptosis. In this review, we highlight the role of cathepsins in these signalling pathways as well as their translational potential as therapeutic targets in cardiac disease.

不良心脏重塑在临床上表现为心脏结构（大小、质量和几何形状）和功能的有害变化。这些变化，包括心室壁厚度的改变、心室扩张和收缩力差，非常重要，因为它们逐渐导致心脏病患者出现心力衰竭，并与不良预后相关。半胱氨酸组织蛋白酶有助于参与不良心脏重塑的关键信号通路，包括心脏细胞外基质（ECM）的合成和降解、心肌细胞肥大、心肌细胞收缩力受损和细胞凋亡。在这篇综述中，我们强调了组织蛋白酶在这些信号通路中的作用以及它们作为心脏病治疗靶点的转化潜力。