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1. Full Text Effect of microRNA‐26a on vascular endothelial cell injury caused by lower extremity ischemia–reperfusion injury through the AMPK pathway by targeting PFKFB3
by Wu, Ye and Zhang, Min‐Hong and Xue, Yan and Zhang, Tao and Wu, Na and Guo, Wei and Du, Xin and Xu, Yong‐Le
Journal of cellular physiology, ISSN 0021-9541, 03/2019, Volume 234, Issue 3, pp. 2916 - 2928
microRNA‐26a | PFKFB3 | vascular endothelial cell injury | ischemia–reperfusion injury | AMPK pathway | microRNA-26a | Physiology | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Cell Proliferation - genetics | Reperfusion Injury - pathology | Endothelial Cells - metabolism | Gene Expression Regulation - genetics | Humans | Rats | Apoptosis - genetics | Male | Signal Transduction - genetics | von Willebrand Factor - genetics | Nitric Oxide Synthase Type III - genetics | Phosphorylation - genetics | Animals | Nitric Oxide - genetics | Phosphofructokinase-2 - genetics | Superoxide Dismutase-1 - genetics | MicroRNAs - genetics | Thrombomodulin - genetics | Endothelial Cells - pathology | Reperfusion Injury - genetics | Reperfusion Injury - metabolism | AMP-Activated Protein Kinases - genetics | Disease Models, Animal | Endothelin | MicroRNA | Analysis | Nitric oxide | Von Willebrand factor | Genetic engineering | Superoxide | Fructose | Reperfusion injury | Endothelium | Cell proliferation | Phosphorylation | Animal models | Superoxide dismutase | Kinases | Tissues | Proteins | Reperfusion | Ischemia | Restoration | miRNA | Thrombomodulin | Injuries | Adenosine monophosphate | AMP | Ribonucleic acid--RNA | Malondialdehyde | Nitric-oxide synthase | Endothelial cells | Polymerase chain reaction | Gene silencing | Cell injury | Protein kinase | Adenosine kinase | Vascular tissue | Index Medicus
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2. Full Text Brg1-mediated Nrf2/HO-1 pathway activation alleviates hepatic ischemia-reperfusion injury
by Ge, Mian and Yao, Weifeng and Yuan, Dongdong and Zhou, Shaoli and Chen, Xi and Zhang, Yihan and Li, Haobo and Xia, Zhengyuan and Hei, Ziqing
Cell death & disease, ISSN 2041-4889, 06/2017, Volume 8, Issue 6, pp. e2841 - e2841
Life Sciences & Biomedicine | Science & Technology | Cell Biology | Chromatin - metabolism | Heme Oxygenase-1 - metabolism | Liver - pathology | Luciferases - metabolism | Protoporphyrins - pharmacology | Hepatocytes - pathology | Hepatocytes - metabolism | NAD(P)H Dehydrogenase (Quinone) - genetics | Luciferases - genetics | Heme Oxygenase-1 - genetics | Adenoviridae - genetics | NF-E2-Related Factor 2 - genetics | Membrane Proteins - metabolism | Nuclear Proteins - genetics | DNA Helicases - genetics | Reperfusion Injury - genetics | Reperfusion Injury - metabolism | Genes, Reporter | Chromatin - chemistry | Cell Line | Promoter Regions, Genetic | Genetic Vectors - chemistry | Reperfusion Injury - pathology | Signal Transduction | Membrane Proteins - genetics | Liver - metabolism | Gene Expression Regulation | Genetic Vectors - metabolism | Mice, Transgenic | Nuclear Proteins - metabolism | Transcription Factors - genetics | Heme Oxygenase-1 - antagonists & inhibitors | Protein Transport | Transcription Factors - metabolism | DNA Helicases - metabolism | Animals | Membrane Proteins - antagonists & inhibitors | Active Transport, Cell Nucleus - drug effects | NF-E2-Related Factor 2 - metabolism | NAD(P)H Dehydrogenase (Quinone) - metabolism | Mice | Adenoviridae - metabolism | BRG1 protein | Immunoprecipitation | Liver diseases | Liver | Heme oxygenase (decyclizing) | Regulatory sequences | Gene expression | Nuclear transport | Chromatin remodeling | Oxygenase | Transfection | Reperfusion | Ischemia | Hepatocytes | Cellular biology | Rodents | Heme | Hypoxia | Brahma-related gene | NRF2 protein | Index Medicus | Original
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3. Full Text The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury
by Sandanger, Øystein and Ranheim, Trine and Vinge, Leif Erik and Bliksøen, Marte and Alfsnes, Katrine and Finsen, Alexandra V and Dahl, Christen P and Askevold, Erik T and Florholmen, Geir and Christensen, Geir and Fitzgerald, Katherine A and Lien, Egil and Valen, Guro and Espevik, Terje and Aukrust, Pål and Yndestad, Arne
Cardiovascular research, ISSN 0008-6363, 07/2013, Volume 99, Issue 1, pp. 164 - 174
Heart | Myocardial infarction | Inflammasome | Ischaemia-reperfusion | IL-1β | Potassium - metabolism | Up-Regulation | Inflammasomes - metabolism | Cytoskeletal Proteins - genetics | NLR Family, Pyrin Domain-Containing 3 Protein | Caspase 1 - metabolism | Male | NF-kappa B - metabolism | Interleukin-1beta - genetics | RNA, Messenger - metabolism | Myocardial Reperfusion Injury - pathology | Time Factors | Interleukin-1beta - metabolism | Adenosine Triphosphate - metabolism | Myocardial Infarction - physiopathology | Toll-Like Receptors - metabolism | Myocardial Reperfusion Injury - genetics | Disease Models, Animal | Fibroblasts - metabolism | Myocardial Reperfusion Injury - immunology | Rats | Receptors, Cytoplasmic and Nuclear - genetics | Myocardial Infarction - metabolism | Myocardial Reperfusion Injury - physiopathology | Mice, Knockout | Fibroblasts - drug effects | Lipopolysaccharides - pharmacology | Fibroblasts - immunology | Heart Ventricles - metabolism | Mice | Interleukin-18 - genetics | Interleukin-18 - metabolism | Myocardial Reperfusion Injury - prevention & control | Heart Ventricles - drug effects | Receptors, Cytoplasmic and Nuclear - metabolism | Myocardial Infarction - genetics | Rats, Wistar | Ventricular Function, Left | Heart Ventricles - immunology | Myocardial Infarction - immunology | Cytoskeletal Proteins - deficiency | Myocardial Infarction - pathology | Heart Ventricles - pathology | Myocardial Contraction | Mice, Inbred C57BL | Cells, Cultured | Inflammasomes - genetics | Carrier Proteins - genetics | Myocardial Reperfusion Injury - metabolism | Animals | Apoptosis Regulatory Proteins | Carrier Proteins - metabolism | Heart Ventricles - physiopathology | CARD Signaling Adaptor Proteins | Apoptosis | Index Medicus
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4. Full Text Cell death in the kidney
by Priante, Giovanna and Gianesello, Lisa and Ceol, Monica and Del Prete, Dorella and Anglani, Franca
International journal of molecular sciences, ISSN 1661-6596, 07/2019, Volume 20, Issue 14, p. 3598
Glomerular injury | Regulated necrosis | Kidney injury | Tubular injury | Apoptosis | Necrosis | Biochemistry & Molecular Biology | Physical Sciences | Chemistry | Life Sciences & Biomedicine | Chemistry, Multidisciplinary | Science & Technology | Calcinosis - genetics | Epithelial Cells - metabolism | Kidney - pathology | Pyroptosis - drug effects | Apoptosis - drug effects | Epithelial Cells - drug effects | Humans | Reperfusion Injury - drug therapy | Immunogenic Cell Death - drug effects | Apoptosis - genetics | Acute Kidney Injury - genetics | Necrosis - pathology | Kidney - metabolism | Mitochondrial Transmembrane Permeability-Driven Necrosis - genetics | Protective Agents - pharmacology | Apoptosis Regulatory Proteins - genetics | Mitochondrial Transmembrane Permeability-Driven Necrosis - drug effects | Calcinosis - metabolism | Reperfusion Injury - genetics | Reperfusion Injury - metabolism | Necroptosis - drug effects | Ferroptosis - genetics | Ferroptosis - drug effects | Immunogenic Cell Death - genetics | Kidney - drug effects | Reperfusion Injury - pathology | Acute Kidney Injury - drug therapy | Acute Kidney Injury - pathology | Apoptosis Regulatory Proteins - classification | Gene Expression Regulation | Epithelial Cells - pathology | Necrosis - metabolism | Necrosis - prevention & control | Pyroptosis - genetics | Apoptosis Regulatory Proteins - metabolism | Necroptosis - genetics | Animals | Calcinosis - prevention & control | Necrosis - genetics | Acute Kidney Injury - metabolism | Calcinosis - pathology | Kidneys | Epithelial cells | Cell division | Inflammation | Kinases | Autophagy | Nephrons | Embryogenesis | Cell growth | Pathways | Ischemia | Cell death | Morphology | Physiology | Kidney diseases | Index Medicus | apoptosis | tubular injury | kidney injury | necrosis | regulated necrosis | glomerular injury
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5. Full Text C/EBP Transcription Factors Mediate Epicardial Activation During Heart Development and Injury
by Guo N. Huang and Jeffrey E. Thatcher and John McAnally and Yongli Kong and Xiaoxia Qi and Wei Tan and J. Michael DiMaio and James F. Amatruda and Robert D. Gerard and Joseph A. Hill and Rhonda Bassel-Duby and Eric N. Olson
Science (American Association for the Advancement of Science), ISSN 0036-8075, 12/2012, Volume 338, Issue 6114, pp. 1599 - 1603
Heart | Transcription factors | HEK293 cells | Transgenic animals | RESEARCH ARTICLES | Neutrophils | Epicardium | Physical trauma | Gene expression | Embryos | Transgenic plants | Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Fundamental and applied biological sciences. Psychology | Biological and medical sciences | Cell physiology | Molecular and cellular biology | Cell differentiation, maturation, development, hematopoiesis | Myocardial Infarction - genetics | WT1 Proteins - metabolism | Oligonucleotide Array Sequence Analysis | Heart - embryology | Male | Pericardium - metabolism | Neutrophil Infiltration | Ventricular Remodeling | Gene Expression Regulation, Developmental | Uroplakin III - genetics | Pericardium - embryology | Female | CCAAT-Enhancer-Binding Protein-delta - metabolism | CCAAT-Enhancer-Binding Proteins - genetics | Binding Sites | Myocardial Reperfusion Injury - genetics | WT1 Proteins - genetics | Organ Culture Techniques | CCAAT-Enhancer-Binding Proteins - metabolism | Heart - physiopathology | Myocardial Contraction | Signal Transduction | CCAAT-Enhancer-Binding Protein-beta - genetics | Gene Expression Regulation | Mice, Transgenic | Aldehyde Oxidoreductases - genetics | Myocardial Infarction - metabolism | CCAAT-Enhancer-Binding Protein-beta - metabolism | Pericardium - cytology | Aldehyde Oxidoreductases - metabolism | Myocardial Reperfusion Injury - metabolism | Animals | Enhancer Elements, Genetic | CCAAT-Enhancer-Binding Protein-delta - genetics | Mice | Models, Genetic | Uroplakin III - metabolism | Cellular signal transduction | Genetic aspects | Research | Genetic transcription | Regeneration (Biology) | Properties | Observations | Proteins | Signal transduction | Cardiovascular disease | Embryology | Rodents | Index Medicus | Injury prevention | Activation | Mathematical models | Adults | Heart function | Protective | Injuries
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6. Full Text miR-21 in ischemia/reperfusion injury: A double-edged sword?
by Xu, Xialian and Kriegel, Alison J and Jiao, Xiaoyan and Liu, Hong and Bai, Xiaowen and Olson, Jessica and Liang, Mingyu and Ding, Xiaoqiang
Physiological genomics, ISSN 1094-8341, 11/2014, Volume 46, Issue 21, pp. 789 - 797
Angiogenesis | Hypoxia | microRNA | Inflammation | Apoptosis | Physiology | Genetics & Heredity | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Fibrosis - genetics | Kidney - blood supply | Neovascularization, Physiologic - genetics | Humans | Gene Expression Regulation | Cell Survival - genetics | Ischemic Preconditioning | Ischemia - genetics | Stem Cell Transplantation | Hypoxia - genetics | Animals | Inflammation - genetics | MicroRNAs - genetics | MicroRNAs - physiology | Reperfusion Injury - genetics | Index Medicus | hypoxia | apoptosis | MicroRNA | inflammation | angiogenesis
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7. Full Text LINC00520 targeting miR‐27b‐3p regulates OSMR expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway
by Tian, Xinghan and Ji, Yongqiang and Liang, Yafeng and Zhang, Jing and Guan, Lina and Wang, Chunting
Journal of cellular physiology, ISSN 0021-9541, 08/2019, Volume 234, Issue 8, pp. 14221 - 14233
acute kidney injury | PI3K‐AKT | miR‐27b‐3p | OSMR | LINC00520 | miR-27b-3p | PI3K-AKT | Physiology | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Cell Line | Cell Proliferation - genetics | Acute Kidney Injury - pathology | Gene Expression Regulation - genetics | Humans | Rats | Acute Kidney Injury - genetics | RNA, Long Noncoding - genetics | Signal Transduction - genetics | Gene Knockdown Techniques | Phosphatidylinositol 3-Kinases - genetics | Animals | Oncogene Protein v-akt - genetics | MicroRNAs - genetics | Oncostatin M Receptor beta Subunit - genetics | Proteins | Genetic research | MicroRNA | Analysis | Flow cytometry | Kidneys | Pathogenesis | AKT protein | mRNA | Ribonucleic acid--RNA | 1-Phosphatidylinositol 3-kinase | Signal transduction | Reporter gene | Injury prevention | Reperfusion | Ischemia | miRNA | Apoptosis | Index Medicus
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8. Full Text BRG1 regulates NOX gene transcription in endothelial cells and contributes to cardiac ischemia-reperfusion injury
by Li, Zilong and Zhang, Xinjian and Liu, Shuai and Zeng, Sheng and Yu, Liming and Yang, Guang and Guo, Junli and Xu, Yong
Biochimica et biophysica acta. Molecular basis of disease, ISSN 0925-4439, 10/2018, Volume 1864, Issue 10, pp. 3477 - 3486
Epigenetics | Endothelial cell | Transcriptional regulation | NOX | ROS | Biochemistry & Molecular Biology | Biophysics | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Reactive Oxygen Species - metabolism | Epigenesis, Genetic | Humans | Gene Knockdown Techniques | NADPH Oxidases - genetics | Histone Code | Nuclear Proteins - genetics | DNA Helicases - genetics | Reperfusion Injury - genetics | Reperfusion Injury - metabolism | Disease Models, Animal | Cell Line | Promoter Regions, Genetic | Reperfusion Injury - pathology | Endothelial Cells - metabolism | Gene Expression Regulation | Nuclear Proteins - metabolism | Transcription Factors - genetics | Transcription Factors - metabolism | DNA Helicases - metabolism | Animals | Endothelial Cells - cytology | Mice | Histones - metabolism | Jumonji Domain-Containing Histone Demethylases - metabolism | Oxidases | Medical research | Epigenetic inheritance | Chromatin | Genes | DNA binding proteins | Genetic transcription | Reperfusion injury | Endothelium | Medicine, Experimental | Genetic research | Histones | Genetic aspects | Index Medicus
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