Cardiovascular disease is still the leading cause of mortality worldwide. Vascular endothelial dysfunction is viewed as the initial step of most cardiovascular diseases. Many studies have indicated that periodontal pathogens, especially Porphyromonas gingivalis, are closely correlated with vascular endothelial homeostasis, but the function of P. gingivalis and the underlying mechanisms are still elusive. To illuminate the effects and elucidate the mechanisms of P. gingivalis on endothelial structural integrity, we developed P. gingivalis infection models in vivo and in vitro. Endothelial cell proliferation, differentiation and apoptosis were detected. Here, we showed that P. gingivalis can impair endothelial integrity by inhibiting cell proliferation and inducing endothelial mesenchymal transformation and apoptosis of endothelial cells, which reduce the cell levels and cause the endothelium to lose its ability to repair itself. A mechanistic analysis showed that TLR antagonist or NF-κB signalling inhibitor can largely rescue the damaged integrity of the endothelium caused by P. gingivalis, suggesting that TLR-NF-κB signalling plays a vital role in vascular endothelial homeostasis destroyed by P. gingivalis. These results suggest a potential intervention method for the prevention and treatment of cardiovascular disease.

心血管疾病仍然是全世界死亡的主要原因。血管内皮功能障碍被视为大多数心血管疾病的第一步。许多研究表明，牙周致病菌，尤其是牙龈卟啉，是密切相关的血管内皮稳态，但功能牙龈和底层机制仍然难以捉摸。为了阐明牙龈卟啉单胞菌对内皮结构完整性的影响并阐明其机制，我们在体内和体外开发了牙龈卟啉单胞菌感染模型。检测内皮细胞增殖、分化和凋亡。在这里，我们展示了P. gingivalis可通过抑制细胞增殖和诱导内皮细胞间充质转化和凋亡来损害内皮完整性，从而降低细胞水平并导致内皮失去自我修复能力。机理分析表明，TLR 拮抗剂或 NF-κB 信号抑制剂可以在很大程度上挽救牙龈卟啉单胞菌引起的内皮完整性受损，表明 TLR-NF-κB 信号传导在牙龈卟啉单胞菌破坏的血管内皮稳态中起着至关重要的作用。这些结果为预防和治疗心血管疾病提供了一种潜在的干预方法。