Chermiti Rania, Burtey Stéphane, Dou Laetitia
C2VN, Aix-Marseille University, INSERM, INRAE, 13005 Marseille, France.
Centre de Néphrologie et Transplantation Rénale, APHM, Hôpital Conception, 13005 Marseille, France.
J Clin Med. 2024 Nov 26;13(23):7149. doi: 10.3390/jcm13237149.
Cardiovascular disease (CVD) is a major complication of chronic kidney disease (CKD), despite improvements in patient care. Vascular inflammation is a crucial process in the pathogenesis of CVD and a critical factor in the cardiovascular complications in CKD patients. CKD promotes a pro-inflammatory environment that impacts the vascular wall, leading to endothelial dysfunction, increased oxidative stress, and vascular remodeling. The uremic toxins that accumulate as kidney function declines are key contributors to vascular inflammatory processes. Our review will examine how CKD leads to vascular inflammation, paving the way to CVD. We will provide an overview of the mechanisms of vascular inflammation induced by uremic toxins, with a particular focus on those derived from tryptophan metabolism. These toxins, along with their receptor, the aryl hydrocarbon receptor (AHR), have emerged as key players linking inflammation and thrombosis. A deeper understanding of the mechanisms underlying inflammation in CKD, particularly those driven by uremic toxins, could reveal valuable therapeutic targets to alleviate the burden of CVD in CKD patients.
尽管患者护理有所改善,但心血管疾病(CVD)仍是慢性肾脏病(CKD)的主要并发症。血管炎症是CVD发病机制中的关键过程,也是CKD患者心血管并发症的关键因素。CKD会促进影响血管壁的促炎环境,导致内皮功能障碍、氧化应激增加和血管重塑。随着肾功能下降而积累的尿毒症毒素是血管炎症过程的关键促成因素。我们的综述将探讨CKD如何导致血管炎症,为CVD的发生铺平道路。我们将概述尿毒症毒素诱导血管炎症的机制,特别关注那些源自色氨酸代谢的毒素。这些毒素及其受体芳烃受体(AHR)已成为连接炎症和血栓形成的关键因素。深入了解CKD炎症的潜在机制,特别是那些由尿毒症毒素驱动的机制,可能会揭示减轻CKD患者CVD负担的有价值的治疗靶点。