Cardiac fibrosis represents an enormous health concern as it is prevalent in nearly every form of cardiovascular disease, the leading cause of death worldwide. Fibrosis is characterized by the activation of fibroblasts into myofibroblasts, a contractile cell type that secretes significant amounts of extracellular matrix components; however, the onset of this condition is also due to persistent inflammation and the cellular responses to a changing mechanical environment. In this review, we provide an overview of the pro-fibrotic, pro-inflammatory, and biomechanical mechanisms that lead to cardiac fibrosis in cardiovascular diseases. We then discuss cadherin-11, an intercellular adhesion protein present on both myofibroblasts and inflammatory cells, as a potential link for all three of the fibrotic mechanisms. Since experimentally blocking cadherin-11 dimerization prevents fibrotic diseases including cardiac fibrosis, understanding how this protein can be targeted for therapeutic use could lead to better treatments for patients with heart disease.

心脏纤维化代表了一个巨大的健康问题，因为它在几乎所有形式的心血管疾病中都很普遍，是全球死亡的主要原因。纤维化的特征是成纤维细胞活化成肌成纤维细胞，肌成纤维细胞是一种可分泌大量细胞外基质成分的收缩细胞类型；然而，这种情况的发生也是由于持续的炎症和细胞对不断变化的机械环境的反应。在这篇综述中，我们概述了导致心血管疾病中心脏纤维化的促纤维化、促炎和生物力学机制。然后，我们讨论了 cadherin-11，一种存在于肌成纤维细胞和炎症细胞上的细胞间粘附蛋白，作为所有三种纤维化机制的潜在联系。