Lipids in health and disease · 2026
Serum YB-1 links dyslipidemia to NET-mediated vascular calcification in hemodialysis.
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Chen Jiaxin, Wang Li, Zhao Shuan, Zhang Jian, Song Nana, Fang Yi, Zhang Zhen, Cao Xuesen, Shen Bo, Teng Jie, Zou Jianzhou, Cai Jieru, Ding Xiaoqiang, Wang Jialin
Аннотация
BACKGROUND: Vascular calcification (VC) is highly prevalent in patients undergoing maintenance hemodialysis (MHD) and is associated with cardiovascular morbidity. However, traditional lipid and mineral markers have limited predictive value. Y-box binding protein-1 (YB-1), a regulator of lipid metabolism and inflammation, may provide additional mechanistic and clinical insight.
METHODS: Serum YB-1 was measured in 209 MHD patients (30-month follow-up) who were stratified into hyperlipidemia and control groups. Receiver Operating Characteristic (ROC) and decision curve analysis (DCA, threshold range 0.1-0.4) were used to assess the predictive performance of YB-1 against traditional models based on lipid, glucose, and bone metabolism. Mechanistic studies in HL-60-derived neutrophil-like cells and a 5/6 nephrectomized rat model were performed to assess the role of YB-1 in neutrophil extracellular trap (NET) formation and VC.
RESULTS: Serum YB-1 was significantly elevated in hyperlipidemia patients and was independently associated with new-onset VC (AUC 0.707, 95% CI 0.630-0.784). YB-1 outperformed lipid-, glucose-, and bone-based models, providing added net clinical benefit in DCA within the 0.24-0.33 threshold range. Mechanistically, serum levels of citrullinated histone H3 (citH3), a NET marker, were increased in hyperlipidemia patients. In vitro, YB-1 and IS synergistically enhanced neutrophil lipid droplet accumulation and citH3 release, while NET-rich supernatants promoted VSMC calcification. In vivo, IS-treated 5/6 nephrectomy rats displayed elevated YB-1, increased citH3, and aggravated aortic calcification.
CONCLUSION: Serum YB-1 is a novel predictor and potential mechanistic mediator of VC in MHD patients. Incorporating YB-1 into existing clinical risk models may support earlier recognition of individuals at elevated cardiovascular risk and inform more effective management strategies to improve long-term health outcomes.
METHODS: Serum YB-1 was measured in 209 MHD patients (30-month follow-up) who were stratified into hyperlipidemia and control groups. Receiver Operating Characteristic (ROC) and decision curve analysis (DCA, threshold range 0.1-0.4) were used to assess the predictive performance of YB-1 against traditional models based on lipid, glucose, and bone metabolism. Mechanistic studies in HL-60-derived neutrophil-like cells and a 5/6 nephrectomized rat model were performed to assess the role of YB-1 in neutrophil extracellular trap (NET) formation and VC.
RESULTS: Serum YB-1 was significantly elevated in hyperlipidemia patients and was independently associated with new-onset VC (AUC 0.707, 95% CI 0.630-0.784). YB-1 outperformed lipid-, glucose-, and bone-based models, providing added net clinical benefit in DCA within the 0.24-0.33 threshold range. Mechanistically, serum levels of citrullinated histone H3 (citH3), a NET marker, were increased in hyperlipidemia patients. In vitro, YB-1 and IS synergistically enhanced neutrophil lipid droplet accumulation and citH3 release, while NET-rich supernatants promoted VSMC calcification. In vivo, IS-treated 5/6 nephrectomy rats displayed elevated YB-1, increased citH3, and aggravated aortic calcification.
CONCLUSION: Serum YB-1 is a novel predictor and potential mechanistic mediator of VC in MHD patients. Incorporating YB-1 into existing clinical risk models may support earlier recognition of individuals at elevated cardiovascular risk and inform more effective management strategies to improve long-term health outcomes.