16 results on '"Lu, Shan"'
Search Results
2. Role of oral microbiota in atherosclerosis
- Author
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Liu, Xiang-Rui, Xu, Qian, Xiao, Jun, Deng, Yi-Ming, Tang, Zhi-Han, Tang, Ya-Ling, and Liu, Lu-Shan
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- 2020
- Full Text
- View/download PDF
3. Macrophage polarization in atherosclerosis
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Yang, Sai, Yuan, Hou-Qin, Hao, Ya-Meng, Ren, Zhong, Qu, Shun-Lin, Liu, Lu-Shan, Wei, Dang-Heng, Tang, Zhi-Han, Zhang, Ji-Feng, and Jiang, Zhi-Sheng
- Published
- 2020
- Full Text
- View/download PDF
4. PCSK9: A new participant in lipophagy in regulating atherosclerosis?
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Xiao, Jun, Deng, Yi-Min, Liu, Xiang-Rui, Cao, Jian-Ping, Zhou, Min, Tang, Ya-Ling, Xiong, Wen-Hao, Jiang, Zhi-Sheng, Tang, Zhi-Han, and Liu, Lu-Shan
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- 2019
- Full Text
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5. Role of oral microbiota in atherosclerosis
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Ya-Ling Tang, Zhi-Han Tang, Lu-Shan Liu, Xiang-Rui Liu, Qian Xu, Yiming Deng, and Jun Xiao
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0301 basic medicine ,Clinical Biochemistry ,Inflammation ,Disease ,Gut flora ,Systemic inflammation ,Biochemistry ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,Animals ,Humans ,Macrophage ,Foam cell ,Mouth ,biology ,business.industry ,Cholesterol ,Microbiota ,Biochemistry (medical) ,General Medicine ,Atherosclerosis ,biology.organism_classification ,stomatognathic diseases ,030104 developmental biology ,chemistry ,030220 oncology & carcinogenesis ,Immunology ,medicine.symptom ,business ,Lipoprotein - Abstract
Oral infections are common among individuals of all ages and can activate local and systemic inflammation. The inflammatory response plays an important role in atherosclerosis. An increasing number of studies have reported an association between oral pathogen infection and atherosclerotic coronary heart disease. For instance, epidemiological studies support the positive correlation between oral infections and atherosclerosis. The presence of oral pathogens in human atherosclerotic plaques has been detected by multiple methods, and oral infections promote atherosclerosis in animal experiments. Various mechanisms are involved in oral infections, thereby promoting atherosclerosis. First, oral infections can trigger the local and systemic inflammatory response, causing vascular endothelial damage. Oral-derived pathogens that enter atherosclerotic plaque can activate macrophages and cause an intra-plaque inflammatory response. Second, oral infections can promote intra-plaque macrophage cholesterol accumulation and foam cell formation. Third, oral infections can regulate plasma lipid levels, thereby increasing atherogenic lipid low-density lipoprotein and triglyceride levels. Although atherosclerosis caused by oral infections is currently studied, the precise mechanism remains to be further explored. The rise of gut microbiota research also makes the relationship between oral microbiota and disease, especially the relationship with coronary heart disease, worthy of attention and in-depth research.
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- 2020
6. Macrophage polarization in atherosclerosis
- Author
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Sai Yang, Jifeng Zhang, Shun-Lin Qu, Zhong Ren, Ya-Meng Hao, Lu-Shan Liu, Dang-Heng Wei, Zhi-Han Tang, Hou-Qin Yuan, and Zhi-Sheng Jiang
- Subjects
0301 basic medicine ,Vascular smooth muscle ,Atherosclerotic cardiovascular disease ,business.industry ,Macrophages ,Biochemistry (medical) ,Clinical Biochemistry ,Macrophage polarization ,General Medicine ,Macrophage Activation ,Atherosclerosis ,Biochemistry ,Phenotype ,Pathogenesis ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,030220 oncology & carcinogenesis ,Immunology ,Chronic inflammatory response ,Animals ,Humans ,Macrophage ,Medicine ,business - Abstract
Atherosclerosis is a chronic inflammatory response that increases the risk of cardiovascular diseases. An in-depth study of the pathogenesis of atherosclerosis is critical for the treatment of atherosclerotic cardiovascular disease. The development of atherosclerosis involves many cells, such as endothelial cells, vascular smooth muscle cells, macrophages, and others. The considerable effects of macrophages in atherosclerosis are inextricably linked to macrophage polarization and the resulting phenotype. Moreover, the significant impact of macrophages on atherosclerosis depend not only on the function of the different macrophage phenotypes but also on the relative ratio of different phenotypes in the plaque. Research on atherosclerosis therapy indicates that the reduced plaque size and enhanced stability are partly due to modulating macrophage polarization. Therefore, regulating macrophage polarization and changing the proportion of macrophage phenotypes in plaques is a new therapeutic approach for atherosclerosis. This review provides a new perspective for atherosclerosis therapy by summarizing the relationship between macrophage polarization and atherosclerosis, as well as treatment targeting macrophage polarization.
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- 2020
7. Tissue factor pathway inhibitor in atherosclerosis
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Bin-Jie Yan, Zhi-Sheng Jiang, Feng-Tao Liu, Zhong Ren, Zhi-Han Tang, Hong-Feng Gu, Hou-Qin Yuan, Lu-Shan Liu, Da-Xing Chen, Ya-Meng Hao, and Shun-Lin Qu
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0301 basic medicine ,Vascular smooth muscle ,business.industry ,Mechanism (biology) ,Lipoproteins ,Biochemistry (medical) ,Clinical Biochemistry ,Cell ,General Medicine ,Atherosclerosis ,Biochemistry ,Endothelial stem cell ,Extracellular matrix ,03 medical and health sciences ,Tissue factor ,030104 developmental biology ,0302 clinical medicine ,medicine.anatomical_structure ,Tissue factor pathway inhibitor ,Coagulation ,030220 oncology & carcinogenesis ,medicine ,Cancer research ,Humans ,business - Abstract
Tissue factor pathway inhibitor (TFPI) reduces the development of atherosclerosis by regulating tissue factor (TF) mediated coagulation pathway. In this review, we focus on recent findings on the inhibitory effects of TFPI on endothelial cell activation, vascular smooth muscle cell (VSMC) proliferation and migration, inflammatory cell recruitment and extracellular matrix which are associated with the development of atherosclerosis. Meanwhile, we are also concerned about the impact of TFPI levels and genetic polymorphisms on clinical atherogenesis. This article aims to explain the mechanism in inhibiting the development of atherosclerosis and clinical effects of TFPI, and provide new ideas for the clinical researches and mechanism studies of atherothrombosis.
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- 2019
8. Endothelial to mesenchymal transition in atherosclerotic vascular remodeling
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Shun-Lin Qu, Ya-Meng Hao, Lu-Shan Liu, Mingui Fu, Kai Yin, Hou-Qin Yuan, Dang-HengWei, Zhi-Sheng Jiang, and Zhong Ren
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0301 basic medicine ,Epithelial-Mesenchymal Transition ,Endothelium ,Clinical Biochemistry ,Vascular Remodeling ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,Transforming Growth Factor beta ,medicine ,Humans ,Endothelial dysfunction ,Neovascularization, Pathologic ,business.industry ,Biochemistry (medical) ,Mesenchymal stem cell ,General Medicine ,Atherosclerosis ,medicine.disease ,Phenotype ,Endothelial stem cell ,030104 developmental biology ,Lymphatic system ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Cancer research ,Myocardial fibrosis ,Signal transduction ,business - Abstract
Endothelial cells are the main components of the heart, blood vessels, and lymphatic vessels, which play an important role in regulating the physiological functions of the cardiovascular system. Endothelial dysfunction is involved in a variety of acute and chronic cardiovascular diseases. As a special type of epithelial-mesenchymal transition (EMT), endothelium to mesenchymal transition (EndMT) regulates the transformation of endothelial cells into mesenchymal cells accompanied by changes in the expression of various transcription factors and cytokines, which is closely related to vascular endothelial injury, vascular remodeling, myocardial fibrosis and valvar disease. Endothelial cells undergoing EndMT lose their endothelial characteristics and undergo a transition toward a more mesenchymal-like phenotype. However, the molecular mechanism of EndMT remains unclear. EndMT, as a type of endothelial dysfunction, can cause vascular remodeling which is a major determinant of atherosclerotic luminal area. Therefore, exploring the important signaling pathways in the process of EndMT may provide novel therapeutic strategies for treating atherosclerotic diseases.
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- 2019
9. PCSK9: A potential regulator of apoE/apoER2 against inflammation in atherosclerosis?
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Hong-yan Wen, Xue-qin Bai, Mei-mei Wang, Qiong Xiang, Juan Peng, Zhi-Han Tang, Zhong Ren, Lu-Shan Liu, Jun Xiao, and Zhi-Sheng Jiang
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0301 basic medicine ,Apolipoprotein E ,medicine.medical_specialty ,Low-density lipoprotein receptor-related protein 8 ,Clinical Biochemistry ,Inflammation ,030204 cardiovascular system & hematology ,Biochemistry ,03 medical and health sciences ,Apolipoproteins E ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,Receptor ,LDL-Receptor Related Proteins ,Chemistry ,PCSK9 ,Biochemistry (medical) ,Lipid metabolism ,General Medicine ,Atherosclerosis ,030104 developmental biology ,Endocrinology ,LDL receptor ,lipids (amino acids, peptides, and proteins) ,Proprotein Convertase 9 ,medicine.symptom ,Lipoprotein - Abstract
Atherosclerosis is characterized by chronic inflammation and lipid accumulation in arterial walls, resulting in several vascular events. Proprotein convertase subtilisin kexin 9 (PCSK9), a serine protease, has a pivotal role in the degradation of hepatic low-density lipoprotein receptor (LDLR). It can increase plasma concentrations of low-density lipoprotein cholesterol and affect lipid metabolism. Recently, PCSK9 has been found to accelerate atherosclerosis via mechanisms apart from that involving the degradation of LDLR, with an emerging role in regulating the inflammatory response in atherosclerosis. Apolipoprotein E receptor 2 (apoER2), one of the LDLR family members expressed in macrophages, can bind to its ligand apolipoprotein E (apoE), exhibiting an anti-inflammatory role in atherosclerosis. Evidence suggests that apoER2 is a target of PCSK9. This review aims to discuss PCSK9 as a potential regulator of apoE/apoER2 against inflammation in atherosclerosis.
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- 2018
10. Functional regulatory roles of microRNAs in atherosclerosis
- Author
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Qing Li, Zhi-Sheng Jiang, Guixue Wang, Mei-mei Wang, Ni-Ya He, Lu-Shan Liu, Ya Gao, Xue-shan Zhao, Zhong Ren, Hong-yan Wen, Juan Peng, and Zhi-Han Tang
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0301 basic medicine ,Vascular smooth muscle ,medicine.medical_treatment ,Clinical Biochemistry ,Cell ,Inflammation ,Biology ,Biochemistry ,Muscle, Smooth, Vascular ,03 medical and health sciences ,Gene expression ,microRNA ,medicine ,Humans ,Macrophage ,Molecular Targeted Therapy ,Macrophages ,Biochemistry (medical) ,Endothelial Cells ,General Medicine ,Atherosclerosis ,Cell biology ,Endothelial stem cell ,MicroRNAs ,030104 developmental biology ,Cytokine ,medicine.anatomical_structure ,medicine.symptom - Abstract
MicroRNAs are a group of endogenously small non-coding RNA molecules that downregulate gene expression at the post-transcriptional level through binding to the 3'UTR of target mRNAs. Recent findings have revealed a key role for microRNAs in the pathophysiological processes of atherosclerosis. As a complex disease, atherosclerosis is influenced by a combination of multiple genes and environmental factors. Both of them play a role in atherogenesis by affecting different types of cells (such as endothelial cell, vascular smooth muscle cell and monocyte/macrophage) function. MicroRNAs control the senescence and dysfunction of endothelial cells, proliferation and migration of vascular smooth muscle cells, and macrophage-driven cytokine production and polarization. By these effects, microRNAs can influence the processes of atherosclerosis and may represent new molecular targets for therapy.
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- 2016
11. Tissue factor pathway inhibitor in atherosclerosis
- Author
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Yuan, Hou-Qin, primary, Hao, Ya-Meng, additional, Ren, Zhong, additional, Gu, Hong-Feng, additional, Liu, Feng-Tao, additional, Yan, Bin-Jie, additional, Qu, Shun-Lin, additional, Tang, Zhi-Han, additional, Liu, Lu-Shan, additional, Chen, Da-Xing, additional, and Jiang, Zhi-Sheng, additional
- Published
- 2019
- Full Text
- View/download PDF
12. PCSK9: A potential regulator of apoE/apoER2 against inflammation in atherosclerosis?
- Author
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Bai, Xue-qin, primary, Peng, Juan, additional, Wang, Mei-mei, additional, Xiao, Jun, additional, Xiang, Qiong, additional, Ren, Zhong, additional, Wen, Hong-yan, additional, Jiang, Zhi-sheng, additional, Tang, Zhi-han, additional, and Liu, Lu-shan, additional
- Published
- 2018
- Full Text
- View/download PDF
13. Functional regulatory roles of microRNAs in atherosclerosis
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Gao, Ya, primary, Peng, Juan, additional, Ren, Zhong, additional, He, Ni-ya, additional, Li, Qing, additional, Zhao, Xue-shan, additional, Wang, Mei-mei, additional, Wen, Hong-yan, additional, Tang, Zhi-han, additional, Jiang, Zhi-sheng, additional, Wang, Gui-xue, additional, and Liu, Lu-shan, additional
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- 2016
- Full Text
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14. Imbalanced cholesterol metabolism in Alzheimer's disease
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Xue-shan, Zhao, primary, juan, Peng, additional, Qi, Wu, additional, Zhong, Ren, additional, Li-hong, Pan, additional, Zhi-han, Tang, additional, Zhi-sheng, Jiang, additional, Gui-xue, Wang, additional, and Lu-shan, Liu, additional
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- 2016
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15. Annexin V− and tissue factor+ microparticles as biomarkers for predicting deep vein thrombosis in patients after joint arthroplasty.
- Author
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Chen, Yuying, Liu, Jian, Su, Yu, Zhao, Huiru, Zhao, Yujing, Wen, Meng, Lu, Shan, Cao, Xiangyu, Zhang, Wenjie, Liu, Lei, and Wu, Jun
- Subjects
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ARTHROPLASTY , *VENOUS thrombosis , *VENA cava inferior , *THROMBOEMBOLISM , *TRANSMISSION electron microscopy , *ANNEXINS - Abstract
• We measured a wide range of MP subpopulations. • The clinical samples are from joint arthroplasty patients rather than mouse cancer models or inferior vena cava (IVC) ligation models. • The collected data on MPs in patients before and after joint arthroplasty at continuous time points. • Annexin V- and tissue factor+ microparticles are good biomarkers for diagnosing VTE during the early phase of postoperative joint arthroplasty. • Microparticles is easier and more convenient to be measured compared to ultrasound and venography. Venous thromboembolism (VTE) is a common and severe complication of joint arthroplasty. Microparticles (MPs) containing phosphatidylserine (PS) and tissue factor (TF) can trigger coagulation in VTE. This study aims to measure and compare MP levels in joint arthroplasty patients with and without VTE. This prospective cohort study enrolled 181 patients who underwent joint arthroplasty. Ultrasound examination was used to diagnose VTE on preoperative day 0 and postoperative day 6. MPs were analysed using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and flow cytometry. The levels of platelet-derived microparticles (PMPs), endothelial cell-derived microparticles (EMPs), granulocyte-derived microparticles (GMPs), red cell-derived microparticles (RMPs), monocyte-derived microparticles (MMPs), Annexin V+ MPs (AV+ MPs), and tissue factor+ MPs (TF+ MPs) derived from five kinds of MPs were measured on day 0 (before surgery), 1, 2, 3, 4, 5, and 6 after surgery. The levels of AV-TF+ EMPs and AV-TF+ MMPs were significantly increased in patients with VTE on postoperative day 5 compared to those without VTE (P = 0.031 and P = 0.031, respectively). AV-TF+ MPs may indicate the development of VTE and serve as predictive markers in joint arthroplasty patients. [ABSTRACT FROM AUTHOR]
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- 2022
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16. Endothelial to mesenchymal transition in atherosclerotic vascular remodeling.
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Hao, Ya-Meng, Yuan, Hou-Qin, Ren, Zhong, Qu, Shun-Lin, Liu, Lu-Shan, Dang-HengWei, Yin, Kai, Fu, Mingui, and Jiang, Zhi-Sheng
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VASCULAR remodeling , *MESENCHYMAL stem cells , *ENDOTHELIAL cells , *CARDIOVASCULAR system , *CARDIOVASCULAR diseases - Abstract
Abstract Endothelial cells are the main components of the heart, blood vessels, and lymphatic vessels, which play an important role in regulating the physiological functions of the cardiovascular system. Endothelial dysfunction is involved in a variety of acute and chronic cardiovascular diseases. As a special type of epithelial-mesenchymal transition (EMT), endothelium to mesenchymal transition (EndMT) regulates the transformation of endothelial cells into mesenchymal cells accompanied by changes in the expression of various transcription factors and cytokines, which is closely related to vascular endothelial injury, vascular remodeling, myocardial fibrosis and valvar disease. Endothelial cells undergoing EndMT lose their endothelial characteristics and undergo a transition toward a more mesenchymal-like phenotype. However, the molecular mechanism of EndMT remains unclear. EndMT, as a type of endothelial dysfunction, can cause vascular remodeling which is a major determinant of atherosclerotic luminal area. Therefore, exploring the important signaling pathways in the process of EndMT may provide novel therapeutic strategies for treating atherosclerotic diseases. Highlights • EndMT, as a kind of endothelial dysfunction, participates in and affects the complex pathophysiological process of vascular remodeling. • Vascular remodeling is considered to be an important issue in atherosclerotic disease. • It may provide novel therapeutic strategies to explore the signaling pathways in the process of EndMT for treating atherosclerotic diseases. [ABSTRACT FROM AUTHOR]
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- 2019
- Full Text
- View/download PDF
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