Yuanyuan Wei

Second Affiliated Hospital of Zhejiang University

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Yue Wu

Ministry of Education of the People's Republic of China

Zuyi Yuan

Ministry of Education of the People's Republic of China

Gulinigaer Tuerhongjiang

First Affiliated Hospital of Xi'an Jiaotong University

Ying Xiong

Chengdu Women's and Children's Central Hospital

Hui Liu

Liaoning Technical University

Hui Luan

Xi'an Jiaotong University

Bo Zhou

First Affiliated Hospital of Xi'an Jiaotong University

Tao Zheng

First Affiliated Hospital of Xi'an Jiaotong University

Xiao Yuan

Shandong First Medical University

Peining Liu

First Affiliated Hospital of Xi'an Jiaotong University

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First Affiliated Hospital of Xi'an Jiaotong University

Ministry of Education of the People's Republic of China

Xi'an Jiaotong University

Sir Run Run Shaw Hospital

Central South University

China-Japan Friendship Hospital

Peking University

Jiangnan University

Qingdao University

Capital Medical University

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GSDME-mediated pyroptosis promotes the progression and associated inflammation of atherosclerosis

Nature Communications (2023)

Yuanyuan Wei Di Lan Tao Zheng Lin Yang Xiaoxia Zhang

Abstract Pyroptosis, a type of Gasdermin-mediated cell death, contributes to an exacerbation of inflammation. To test the hypothesis that GSDME-mediated pyroptosis aggravates the progression of atherosclerosis, we generate ApoE and GSDME dual deficiency mice. As compared with the control mice, GSDME −/− /ApoE −/− mice show a reduction of atherosclerotic lesion area and inflammatory response when induced with a high-fat diet. Human atherosclerosis single-cell transcriptome analysis demonstrates that GSDME is mainly expressed in macrophages. In vitro, oxidized low-density lipoprotein (ox-LDL) induces GSDME expression and pyroptosis in macrophages. Mechanistically, ablation of GSDME in macrophages represses ox-LDL-induced inflammation and macrophage pyroptosis. Moreover, the signal transducer and activator of transcription 3 (STAT3) directly correlates with and positively regulates GSDME expression. This study explores the transcriptional mechanisms of GSDME during atherosclerosis development and indicates that GSDME-mediated pyroptosis in the progression of atherosclerosis could be a potential therapeutic approach for atherosclerosis.

Pyroptosis

Foam cell

Clusterin

10.1038/s41467-023-36614-w

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Gut Microbiota Regulate Saturated Free Fatty Acid Metabolism in Heart Failure

Small Science (2024)

Gulinigaer Tuerhongjiang Manyun Guo Xiangrui Qiao Junhui Liu Xi Wen

Aims: Heart failure (HF) is associated with profound changes in cardiac metabolism. At present, there is still a lack of relevant research to explore the key microbiome and their metabolites affecting the progression of HF. Herein, the interaction of gut microbiota and circulating free fatty acid (FFA) in HF patients and mice is investigated. Methods and Results: In HF patients, by applying metagenomics analysis and targeted FFA metabolomics, enriched abundance of Clostridium sporogenes ( C.sp ) in early and late stage of HF patients, which negatively correlated to saturated free fatty acid (SFA) levels, is identified. KEGG analysis further indicates microbiota gene enrichment in FFA degradation in early HF, and decreased gene expression in FFA synthesis in late HF. In HF mice (C57BL/6J) induced by isoproterenol (ISO), impaired intestinal permeability is observed, and decreased fecal C.sp and increased SFA are further validated. At last, by supplementing C.sp to ISO‐induced HF mice, the cardiac function, fibrosis, and myocardial size are partially rescued, together with decreased circulating SFA levels. Conclusions: Clostridium abundance is increased in HF, compensating cardiac function deterioration via downregulation of circulating SFA levels. The results demonstrate that the gut microbiota–SFA axis plays an important role in HF protection, which may provide a strategic advantage for the probiotic therapy development in HF.

Fatty Acid Metabolism

10.1002/smsc.202300337

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The association of glycated hemoglobin A1c with coronary artery disease, myocardial infarction, and severity of coronary lesions

Journal of Investigative Medicine (2023)

Yuanyuan Wei Wenyuan Li Hui Luan Gulinigaer Tuerhongjiang Zuyi Yuan

Glycated hemoglobin A1c (HbA1c) has been recognized as a predictor of cardiovascular events. However, the relationship between HbA1c and coronary artery disease (CAD) in the Chinese population has yet to be systematically explored. In addition, factors associated with HbA1c were generally analyzed linearly, thereby failing to appreciate more complex nonlinear associations. The study aimed to evaluate the relationship between the HbA1c value and the presence and severity of coronary artery stenosis. A total of 7192 consecutive patients who underwent coronary angiography were enrolled. Their biological parameters, including HbA1c, were measured. The severity of coronary stenosis was evaluated using Gensini score. After correcting for baseline confounding factors, a multivariate logistic regression analysis was used to evaluate the relationship between HbA1c and CAD severity. Restricted cubic splines were applied to explore the relation of HbA1c with the presence of CAD, myocardial infarction (MI), and the severity of coronary lesions. HbA1c was significantly associated with the presence and severity of CAD in patients without diagnosed diabetes (odds ratio: 1.306, 95% confidence interval: 1.053–1.619, p = 0.015). Spline analysis showed a U-shaped association of HbA1c with the presence of MI. Both HbA1c > 7.2% and HbA1c < 5.7% were associated with the presence of MI. In conclusion, HbA1c value was highly associated with the severity of coronary artery stenosis in the whole study population, and in CAD patients without diagnosed diabetes. Compared with patients with HbA1c levels between 6.0% and 7.0%, HbA1c < 5.7% and HbA1c > 7.2% were associated with higher presence of MI.

Glycated hemoglobin

10.1177/10815589221140593

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Citations (4)