Xuebo Liu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Xuebo Liu has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
Hao Lin
Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China
3 shared publications- Hongwei Tan
Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China
2 shared publications Yuntao Feng
Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China
2 shared publicationsDeqiang Yuan
Department of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China
1 shared publication- Fei Chen
Department of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200333, China
1 shared publication Jiapeng Chu
Department of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China
1 shared publication
Latest Publications
- 16 March 2024
- Published by Elsevier in Clinical Nutrition ESPEN
- Vol. 61, 131-139
Life's essential 8 metrics and mortality outcomes in insulin resistance: The role of inflammation, vascular aging, and gender
- 16 March 2024
- Published by Elsevier in Clinical Nutrition ESPEN
- Vol. 61, 131-139
Life's essential 8 metrics and mortality outcomes in insulin resistance: The role of inflammation, vascular aging, and gender
- Open Access
- 8 March 2024
- Published by Elsevier in The Journal of nutrition, health and aging
- Vol. 28 (5) , 100203
Heterogeneity of aging and mortality risk among individuals with hypertension: Insights from phenotypic age and phenotypic age acceleration
- 8 March 2024
- Published by Elsevier in The Journal of nutrition, health and aging
- Vol. 28 (5) , 100203
Open AccessHeterogeneity of aging and mortality risk among individuals with hypertension: Insights from phenotypic age and phenotypic age acceleration
- Open Access
- 20 September 2023
- Published by Springer Nature in BMC Cardiovascular Disorders
- Vol. 23 (1) , 1-15
MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1
Myocardial infarction (MI) is a leading cause of mortality. To better understand its molecular and cellular mechanisms, we used bioinformatic tools and molecular experiments to explore the pathogenesis and prognostic markers. Differential gene expression analysis was conducted using GSE60993 and GSE66360 datasets. Hub genes were identified through pathway enrichment analysis and PPI network construction, and four hub genes (AQP9, MMP9, FPR1, and TREM1) were evaluated for their predictive performance using AUC and qRT-PCR. miR-206 was identified as a potential regulator of TREM1. Finally, miR-206 was found to induce EC senescence and ER stress through upregulating mitochondrial ROS levels via TREM1. These findings may contribute to understanding the pathogenesis of MI and identifying potential prognostic markers.
- 20 September 2023
- Published by Springer Nature in BMC Cardiovascular Disorders
- Vol. 23 (1) , 1-15
Open AccessMiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1
Myocardial infarction (MI) is a leading cause of mortality. To better understand its molecular and cellular mechanisms, we used bioinformatic tools and molecular experiments to explore the pathogenesis and prognostic markers. Differential gene expression analysis was conducted using GSE60993 and GSE66360 datasets. Hub genes were identified through pathway enrichment analysis and PPI network construction, and four hub genes (AQP9, MMP9, FPR1, and TREM1) were evaluated for their predictive performance using AUC and qRT-PCR. miR-206 was identified as a potential regulator of TREM1. Finally, miR-206 was found to induce EC senescence and ER stress through upregulating mitochondrial ROS levels via TREM1. These findings may contribute to understanding the pathogenesis of MI and identifying potential prognostic markers.