Periodontitis is an autoimmune disease of periodontal tissues initiated by plaque. It is known that there is a close connection between periodontitis and CKD with hypertension, but the underlying mechanisms are unknown. STAT1 has been reported to play a regulatory role in hypertension and chronic kidney disease (CKD). Here, we investigated whether STAT1 regulates periodontitis‐mediated aggravation of kidney injury with accompanying hypertension. A hypertensive renal injury mouse model was established with Nos3 knockout mice, and a periodontitis model was established by implantation with the oral bacteria Porphyromonas gingivalis. The mice were intraperitoneally injected with a STAT1 inhibitor. Periodontitis aggravated kidney injury in hypertensive mice, and upregulation of STAT1 was observed when both periodontitis and hypertension were present; furthermore, STAT1 inhibitor moderated this effect. Moreover, we observed that periodontitis promoted the upregulation of inflammatory and fibrosis gene expression in the kidneys of hypertensive mice. In addition, STAT1 inhibition decreased the expression of pro‐inflammatory and pro‐fibrotic cytokines in the kidney lesion area. Periodontitis augmented the expression of inflammatory and fibrosis genes by upregulating the expression of STAT1, thereby aggravating kidney injury in the hypertensive mouse model.

中文翻译：

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牙周炎通过上调高血压小鼠模型中的 STAT1 表达加重肾损伤

牙周炎是由牙菌斑引发的牙周组织自身免疫性疾病。众所周知，牙周炎和慢性肾病与高血压之间存在密切联系，但其潜在机制尚不清楚。据报道，STAT1 在高血压和慢性肾病 (CKD) 中发挥调节作用。在这里，我们研究了 STAT1 是否调节牙周炎介导的肾损伤加重伴高血压。用Nos3基因敲除小鼠建立高血压肾损伤模型，植入口腔细菌牙龈卟啉单胞菌建立牙周炎模型. 小鼠腹腔注射STAT1抑制剂。牙周炎加重高血压小鼠的肾损伤，当牙周炎和高血压同时存在时，观察到STAT1的上调；此外，STAT1 抑制剂缓和了这种作用。此外，我们观察到牙周炎促进了高血压小鼠肾脏炎症和纤维化基因表达的上调。此外，STAT1抑制降低了肾脏病变区域促炎和促纤维化细胞因子的表达。牙周炎通过上调STAT1的表达增加炎症和纤维化基因的表达，从而加重高血压小鼠模型的肾损伤。