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1,512 results on '"Lin, Shing-Jong"'

3. Long-term administration of Western diet induced metabolic syndrome in mice and causes cardiac microvascular dysfunction, cardiomyocyte mitochondrial damage, and cardiac remodeling involving caveolae and caveolin-1 expression

Author

Liu, I.-Fan, Lin, Tzu-Chieh, Wang, Shu-Chi, Yen, Chia-Hung, Li, Chia-Yang, Kuo, Hsuan-Fu, Hsieh, Chong-Chao, Chang, Chia-Yuan, Chang, Chuang-Rung, Chen, Yung-Hsiang, Liu, Yu-Ru, Lee, Tsung-Ying, Huang, Chi-Yuan, Hsu, Chih-Hsin, Lin, Shing-Jong, and Liu, Po-Len

Published
2023
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5. Inhibition of Serine Protease Activity Protects Against High Fat Diet-Induced Inflammation and Insulin Resistance.

Author

Kuo, Chin-Sung, Chen, Jia-Shiong, Lin, Liang-Yu, Schmid-Schoenbein, Geert, Chien, Shu, Huang, Po-Hsun, Chen, Jaw-Wen, and Lin, Shing-Jong

Subjects
Adult, Aged, Animals, Cross-Sectional Studies, Cytokines, Diabetes Mellitus, Type 2, Diet, High-Fat, Disease Models, Animal, Female, Humans, Inflammation, Inflammation Mediators, Insulin Resistance, Male, Mice, Mice, Knockout, Middle Aged, Receptors, LDL, Serine Proteases, Serine Proteinase Inhibitors
Abstract

Recent evidence suggests that enhanced protease-mediated inflammation may promote insulin resistance and result in diabetes. This study tested the hypothesis that serine protease plays a pivotal role in type 2 diabetes, and inhibition of serine protease activity prevents hyperglycemia in diabetic animals by modulating insulin signaling pathway. We conducted a single-center, cross-sectional study with 30 healthy controls and 57 patients with type 2 diabetes to compare plasma protease activities and inflammation marker between groups. Correlations of plasma total and serine protease activities with variables were calculated. In an in-vivo study, LDLR-/- mice were divided into normal chow diet, high-fat diet (HFD), and HFD with selective serine protease inhibition groups to examine the differences of obesity, blood glucose level, insulin resistance and serine protease activity among groups. Compared with controls, diabetic patients had significantly increased plasma total protease, serine protease activities, and also elevated inflammatory cytokines. Plasma serine protease activity was positively correlated with body mass index, hemoglobin A1c, homeostasis model assessment-insulin resistance index (HOMA-IR), tumor necrosis factor-α, and negatively with adiponectin concentration. In the animal study, administration of HFD progressively increased body weight, fasting glucose level, HOMA-IR, and upregulated serine protease activity. Furthermore, in-vivo serine protease inhibition significantly suppressed systemic inflammation, reduced fasting glucose level, and improved insulin resistance, and these effects probably mediated by modulating insulin receptor and cytokine expression in visceral adipose tissue. Our findings support the serine protease may play an important role in type 2 diabetes and suggest a rationale for a therapeutic strategy targeting serine protease for clinical prevention of type 2 diabetes.

Published
2020

9. 2021 Consensus Pathway of the Taiwan Society of Cardiology on Novel Therapy for Type 2 Diabetes

Author

Chiang, Chern-En, Ueng, Kwo-Chang, Chao, Ting-Hsing, Lin, Tsung-Hsien, Wu, Yih-Jer, Wang, Kang-Ling, Sung, Shih-Hsien, Yeh, Hung-I, Li, Yi-Heng, Liu, Ping-Yen, Chang, Kuan-Cheng, Shyu, Kou-Gi, Huang, Jin-Long, Tsai, Cheng-Dao, Hung, Huei-Fong, Liu, Ming-En, Chao, Tze-Fan, Cheng, Shu-Meng, Cheng, Hao-Min, Chu, Pao-Hsien, Yin, Wei-Hsian, Wu, Yen-Wen, Chen, Wen-Jone, Lai, Wen-Ter, Lin, Shing-Jong, Yeh, San-Jou, Hwang, Juey-Jen, and Hou, Charles Jia-Yin

Published
2021
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13. Myocardial Bridging Increases the Risk of Adverse Cardiovascular Events in Patients without Coronary Atherosclerosis.

Author

Yang, Tsung-Lin, Hao, Wen-Rui, Chen, Chun-Chao, Fang, Yu-Ann, Leu, Hsin-Bang, Liu, Ju-Chi, Lin, Shing-Jong, Horng, Jiun-Lin, and Shih, Chun-Ming

Subjects
MAJOR adverse cardiovascular events, CORONARY artery disease, MYOCARDIAL infarction, CORONARY arteries, CORONARY angiography
Abstract

Background: Myocardial bridging (MB) is a congenital coronary anomaly and an important cause of chest pain. The long-term effects of MB on cardiovascular events remain elusive. Methods: We used the National Health Insurance Research Database of Taiwan to conduct an analysis. All patients who had undergone coronary angiography were considered for inclusion. The primary endpoint was a composite of nonfatal myocardial infarction, nonfatal ischemic stroke, and cardiovascular death. Results: We identified 10,749 patients from 2008 to 2018 and matched them with an equal number of controls by propensity-score matching. The mean follow-up period was 5.78 years. In patients without coronary artery disease, MB increased the risk of the composite endpoint (hazard ratio [HR]: 1.57, 95% confidence interval [CI]: 1.44–1.72, p < 0.001), which was driven by increased risks of nonfatal myocardial infarction and cardiovascular death. In patients with significant coronary artery disease, MB did not increase the risk of major adverse cardiovascular events. MB was identical to insignificant coronary artery disease from the viewpoint of clinical outcomes. Conclusions: The presence of MB significantly increases cardiovascular risks in patients with normal coronary vessels. Atherosclerotic coronary artery disease mitigates the effect of MB on cardiovascular outcomes. MB can be considered an insignificant coronary artery disease equivalent. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Association of variability in uric acid and future clinical outcomes of patient with coronary artery disease undergoing percutaneous coronary intervention

Author

Lim, Su Shen, Yang, Ya-Ling, Chen, Su-Chan, Wu, Cheng-Hsueh, Huang, Shao-Sung, Chan, Wan Leong, Lin, Shing-Jong, Chen, Jaw-Wen, Chou, Chia-Yu, Pan, Ju-Pin, Charng, Min-Ji, Chen, Ying-Hwa, Wu, Tao-Cheng, Lu, Tse-Min, Hsu, Pai-Feng, Huang, Po-Hsun, Cheng, Hao-Min, Huang, Chin-Chou, Sung, Shih-Hsien, Lin, Yenn-Jiang, and Leu, Hsin-Bang

Published
2020
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25. Oxidative Stress Activates Endothelial Innate Immunity via Sterol Regulatory Element Binding Protein 2 (SREBP2) Transactivation of MicroRNA-92a

Author

Chen, Zhen, Wen, Liang, Martin, Marcy, Hsu, Chien-Yi, Fang, Longhou, Lin, Feng-Mao, Lin, Ting-Yang, Geary, McKenna J, Geary, Greg G, Zhao, Yongli, Johnson, David A, Chen, Jaw-Wen, Lin, Shing-Jong, Chien, Shu, Huang, Hsien-Da, Miller, Yury I, Huang, Po-Hsun, and Shyy, John Y-J

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Aging, Biotechnology, Genetics, Cardiovascular, Aetiology, 2.1 Biological and endogenous factors, Aged, Angiotensin II, Animals, Coronary Disease, Endothelial Cells, Endothelium, Vascular, Female, Free Radical Scavengers, Gene Expression Regulation, Genes, Reporter, HEK293 Cells, Human Umbilical Vein Endothelial Cells, Humans, Hydrogen Peroxide, Hypercholesterolemia, Immunity, Innate, Inflammasomes, Interleukin-1beta, Kruppel-Like Factor 4, Lipoproteins, LDL, Male, Mice, Mice, Transgenic, MicroRNAs, Middle Aged, Organometallic Compounds, Oxidative Stress, Recombinant Fusion Proteins, Salicylates, Sterol Regulatory Element Binding Protein 2, Transcriptional Activation, Zebrafish, Zebrafish Proteins, endothelium, inflammasomes, microRNA-92, oxidative stress, sterol regulatory element binding protein 2, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences, Sports science and exercise
Abstract

BackgroundOxidative stress activates endothelial innate immunity and disrupts endothelial functions, including endothelial nitric oxide synthase-derived nitric oxide bioavailability. Here, we postulated that oxidative stress induces sterol regulatory element-binding protein 2 (SREBP2) and microRNA-92a (miR-92a), which in turn activate endothelial innate immune response, leading to dysfunctional endothelium.Methods and resultsUsing cultured endothelial cells challenged by diverse oxidative stresses, hypercholesterolemic zebrafish, and angiotensin II-infused or aged mice, we demonstrated that SREBP2 transactivation of microRNA-92a (miR-92a) is oxidative stress inducible. The SREBP2-induced miR-92a targets key molecules in endothelial homeostasis, including sirtuin 1, Krüppel-like factor 2, and Krüppel-like factor 4, leading to NOD-like receptor family pyrin domain-containing 3 inflammasome activation and endothelial nitric oxide synthase inhibition. In endothelial cell-specific SREBP2 transgenic mice, locked nucleic acid-modified antisense miR-92a attenuates inflammasome, improves vasodilation, and ameliorates angiotensin II-induced and aging-related atherogenesis. In patients with coronary artery disease, the level of circulating miR-92a is inversely correlated with endothelial cell-dependent, flow-mediated vasodilation and is positively correlated with serum level of interleukin-1β.ConclusionsOur findings suggest that SREBP2-miR-92a-inflammasome exacerbates endothelial dysfunction during oxidative stress. Identification of this mechanism may help in the diagnosis or treatment of disorders associated with oxidative stress, innate immune activation, and endothelial dysfunction.

Published
2015

27. Matrix metalloproteinase-9 deficiency attenuates diabetic nephropathy by modulation of podocyte functions and dedifferentiation

Author

Li, Szu-Yuan, Huang, Po-Hsun, Yang, An-Hang, Tarng, Der-Cherng, Yang, Wu-Chang, Lin, Chih-Ching, Chen, Jaw-Wen, Schmid-Schönbein, Geert, and Lin, Shing-Jong

Subjects
Kidney Disease, Diabetes, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Renal and urogenital, Albuminuria, Animals, Cell Dedifferentiation, Cells, Cultured, Cytokines, Diabetes Mellitus, Experimental, Diabetic Nephropathies, Humans, Male, Matrix Metalloproteinase 9, Mice, Mice, Knockout, Podocytes, Up-Regulation, diabetes mellitus, diabetic nephropathy, matrix metalloproteinases, podocyte, Clinical Sciences, Urology & Nephrology
Abstract

Diabetic nephropathy is characterized by excessive deposition of extracellular matrix protein and disruption of the glomerular filtration barrier. Matrix metalloproteinases (MMPs) affect the breakdown and turnover of extracellular matrix protein, suggesting that altered expression of MMPs may contribute to diabetic nephropathy. Here we used an MMP-9 gene knockout mouse model, with in vitro experiments and clinical samples, to determine the possible role of MMP-9 in diabetic nephropathy. After 6 months of streptozotocin-induced diabetes, mice developed markedly increased albuminuria, glomerular and kidney hypertrophy, and thickening of the glomerular basement membrane. Gelatin zymographic analysis and western blotting showed that there was enhanced MMP-9 protein production and activity in the glomeruli. However, MMP-9 knockout in diabetic mice significantly attenuated these nephropathy changes. In cultured podocytes, various cytokines related to diabetic nephropathy including TGF-β1, TNF-α, and VEGF stimulated MMP-9 secretion. Overexpression of endogenous MMP-9 induced podocyte dedifferentiation. MMP-9 also interrupted podocyte cell integrity, promoted podocyte monolayer permeability to albumin, and extracellular matrix protein synthesis. In diabetic patients, the upregulation of urinary MMP-9 concentrations occurred earlier than the onset of microalbuminuria. Thus, MMP-9 seems to play a role in the development of diabetic nephropathy.

Published
2014

28. Sex and Age Differences of Major Cardiovascular Events in Patients After Percutaneous Coronary Intervention

Author

Yang, Ya-Ling, primary, Chen, Su-Chan, additional, Wu, Cheng-Hsueh, additional, Huang, Shao-Sung, additional, Chan, Wan Leong, additional, Lin, Shing-Jong, additional, Chou, Chia-Yu, additional, Chen, Jaw-Wen, additional, Pan, Ju-Pin, additional, Charng, Min-Ji, additional, Chen, Ying-Hwa, additional, Wu, Tao-Cheng, additional, Lu, Tse-Min, additional, Hsu, Pai-Feng, additional, Huang, Po-Hsun, additional, Cheng, Hao-Min, additional, Huang, Chin-Chou, additional, Sung, Shih-Hsien, additional, Lin, Yenn-Jiang, additional, and Leu, Hsin-Bang, additional

Published
2023
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29. 2018 consensus of the Taiwan Society of Cardiology and the Diabetes Association of Republic of China (Taiwan) on the pharmacological management of patients with type 2 diabetes and cardiovascular diseases

Author

Chiang, Chern-En, Lin, Shih-Yi, Lin, Tsung-Hsien, Wang, Tzung-Dau, Yeh, Hung-I, Chen, Jung-Fu, Tsai, Chia-Ti, Hung, Yi-Jen, Li, Yi-Heng, Liu, Ping-Yen, Chang, Kuan-Cheng, Wang, Kang-Ling, Chao, Ting-Hsing, Shyu, Kou-Gi, Yang, Wei-Shiung, Ueng, Kwo-Chang, Chu, Pao-Hsien, Yin, Wei-Hsian, Wu, Yen-Wen, Cheng, Hao-Min, Shin, Shyi-Jang, Huang, Chien-Ning, Chuang, Lee-Ming, Lin, Shing-Jong, Yeh, San-Jou, Sheu, Wayne Huey-Herng, and Lin, Jiunn-Lee

Published
2018
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44. 2020 Consensus of Taiwan Society of Cardiology on the pharmacological management of patients with type 2 diabetes and cardiovascular diseases

Author

Chiang, Chern-En, Ueng, Kwo-Chang, Chao, Ting-Hsing, Lin, Tsung-Hsien, Wu, Yih-Jer, Wang, Kang-Ling, Sung, Shih-Hsien, Yeh, Hung-I, Li, Yi-Heng, Liu, Ping-Yen, Chang, Kuan-Cheng, Shyu, Kou-Gi, Huang, Jin-Long, Tsai, Cheng-Dao, Hung, Huei-Fong, Liu, Ming-En, Chao, Tze-Fan, Cheng, Shu-Meng, Cheng, Hao-Min, Chu, Pao-Hsien, Yin, Wei-Hsian, Wu, Yen-Wen, Chen, Wen-Jone, Lai, Wen-Ter, Lin, Shing-Jong, Yeh, San-Jou, and Hwang, Juey-Jen

Published
2020
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