Vascular calcification is the deposition of hydroxyapatite crystals in the medial or intimal layers of arteries that is usually associated with other pathological conditions including but not limited to chronic kidney disease, atherosclerosis and diabetes. Calcification is an active, cell-regulated process involving the phenotype transition of vascular smooth muscle cells (VSMCs) from contractile to osteoblast/chondrocyte-like cells. Diverse triggers and signal transduction pathways have been identified behind vascular calcification. In this review, we focus on the role of reactive oxygen species (ROS) in the osteochondrogenic phenotype switch of VSMCs and subsequent calcification. Vascular calcification is associated with elevated ROS production. Excessive ROS contribute to the activation of certain osteochondrogenic signal transduction pathways, thereby accelerating osteochondrogenic transdifferentiation of VSMCs. Inhibition of ROS production and ROS scavengers and activation of endogenous protective mechanisms are promising therapeutic approaches in the prevention of osteochondrogenic transdifferentiation of VSMCs and subsequent vascular calcification. The present review discusses the formation and actions of excess ROS in different experimental models of calcification, and the potential of ROS-lowering strategies in the prevention of this deleterious condition.

中文翻译：

---

活性氧对血管钙化的调节

血管钙化是羟基磷灰石晶体在动脉内侧或内膜沉积，通常与其他病理状况有关，包括但不限于慢性肾脏疾病，动脉粥样硬化和糖尿病。钙化是一种活跃的细胞调节过程，涉及血管平滑肌细胞（VSMC）从可收缩型转变为成骨细胞/软骨样细胞的表型转变。在血管钙化的背后已经发现了多种触发因素和信号转导途径。在这篇综述中，我们重点研究活性氧（ROS）在VSMC的骨软骨表型转换和随后钙化中的作用。血管钙化与ROS产生升高有关。过多的ROS会激活某些骨软骨形成信号转导通路，从而加速VSMCs的骨软骨形成转分化。抑制ROS产生和ROS清除剂以及激活内源性保护机制是预防VSMCs骨软骨源性转分化和随后血管钙化的有前途的治疗方法。本综述讨论了钙化的不同实验模型中过量ROS的形成和作用，以及降低ROS的策略在预防这种有害状况方面的潜力。