Periodontal disease has been implicated in the progression of various systemic diseases, including chronic kidney disease (CKD). Recent evidence suggests that infection of Porphyromonas gingivalis , a major periodontal pathogen, may also contribute to vascular calcification in patients with CKD. In the present study, antibody array analysis of serum samples from CKD mice administered with oral P. gingivalis revealed significant alterations in protein expression profiles, with notable interleukin-7 (IL-7) upregulation. We demonstrated that P. gingivalis infection enhances the inorganic phosphate-induced calcification of vascular smooth muscle cells (VSMCs), a pathological process that is characteristically accelerated in CKD. Notably, IL-7 expression was significantly upregulated in the P. gingivalis -stimulated calcification of VSMCs. Moreover, IL-7 knockdown in VSMCs markedly attenuated the P. gingivalis -stimulated calcification of VSMCs and suppressed the expression of osteogenic markers, including alkaline phosphatase and Runt-related transcription factor 2. These findings suggest that IL-7 plays a crucial role in P. gingivalis -stimulated vascular calcification, potentially providing new therapeutic targets for preventing vascular calcification in CKD patients with periodontal infection.

Spinach (Spinacia oleracea L.), a green leafy vegetable, is well known as a functional food due to its biological activities. Vascular calcification is associated with several disease conditions including atherosclerosis, diabetes, and chronic kidney disease (CKD), and is known to raise the risk of cardiovascular diseases related morbidity and mortality. However, there are no previous studies that have investigated the effects of fermented spinach exract (FSE) against aortic and its underlying mechanisms. Therefore, this study investigated the effects and action of possible mechanisms of FSE on inorganic phosphate (PI)-induced vascular calcification in ex vivo mouse aortic rings. PI increased vascular calcification through calcium deposition in ex vivo aortic rings. FSE inhibited calcium accumulation and osteogenic key marker, runt-related transcription factor 2 (Runx2), and bone Morphogenetic Protein 2 (BMP-2) protein expression in ex vivo aortic rings. And, FSE inhibited PI-induced extracellular signal-regulated kinase (ERK) and p38 phosphorylation in ex vivo aortic rings. These results show that FSE can prevent vascular calcification which may be a crucial way for the prevention and treatment of vascular disease association with vascular calcification.