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Circulation (New York, N.Y.), ISSN 0009-7322, 04/2017, Volume 135, Issue 21, pp. 2041 - 2057
BACKGROUND—Hypertensive ventricular remodeling is a common cause of heart failure. However, the molecular mechanisms regulating ventricular remodeling remain... 
Heart failure | Fibroblast | P38 mitogenactivated protein kinases | Activating transcription factor 3 | Cardiac & Cardiovascular Systems | Peripheral Vascular Disease | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Fibroblasts - enzymology | Hypertrophy, Left Ventricular - enzymology | Ventricular Function, Left | Heart Failure - enzymology | Humans | Heart Failure - physiopathology | Male | MAP Kinase Kinase 3 - genetics | Heart Failure - prevention & control | Ventricular Remodeling | Time Factors | Hypertension - chemically induced | p38 Mitogen-Activated Protein Kinases - metabolism | Acetylation | Angiotensin II | Binding Sites | Heart Failure - etiology | Activating Transcription Factor 3 - genetics | Disease Models, Animal | Promoter Regions, Genetic | Genetic Predisposition to Disease | Signal Transduction | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - prevention & control | Activating Transcription Factor 3 - deficiency | Cells, Cultured | Myocardium - pathology | Fibroblasts - pathology | Activating Transcription Factor 3 - metabolism | MAP Kinase Kinase 3 - metabolism | Mice, Knockout | Myocardium - enzymology | Phenotype | Animals | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Fibrosis | Protein Kinase Inhibitors - pharmacology | Histones - metabolism | Hypertrophy, Left Ventricular - physiopathology | Transforming Growth Factor beta - metabolism | Histone Deacetylase 1 - metabolism | Index Medicus | Abridged Index Medicus | heart failure | p38 MAPK | cardiac fibroblast | activating transcription factor 3
Journal Article
Nature (London), ISSN 1476-4687, 04/2018, Volume 556, Issue 7702, pp. 501 - 504
.... The major effects of itaconate on cellular metabolism during macrophage activation have been attributed to the inhibition of succinate dehydrogenase , yet this inhibition alone is not sufficient... 
Succinates - chemistry | Glutathione - metabolism | Humans | I-kappa B Proteins - metabolism | Inflammation - metabolism | Succinates - administration & dosage | Psoriasis - pathology | Inflammation - drug therapy | Female | Succinates - metabolism | Stress, Physiological - drug effects | Interleukin-6 - metabolism | Cytokines - immunology | Psoriasis - drug therapy | Cytokines - metabolism | Mice, Inbred C57BL | Toll-Like Receptors - immunology | Cells, Cultured | Activating Transcription Factor 3 - metabolism | Gene Expression Regulation - drug effects | Macrophages - metabolism | Animals | Succinates - therapeutic use | Keratinocytes - drug effects | Keratinocytes - metabolism | NF-E2-Related Factor 2 - metabolism | Macrophages - drug effects | Mice | Succinates - pharmacology | Phosphorylation | Transcription factors | Transcription | Macrophages | Interleukin 6 | Proteins | Cell activation | Metabolites | Rodents | Toll-like receptors | Inhibition | Stress response | Glutathione | Immune system | Immune response | Psoriasis | Immunoregulation | Activating transcription factor 3 | Medical treatment | Interleukin 12 | Inflammation | Metabolism | Gene expression | Interleukin 17 | Chromatography | Dimethylitaconate | Tumor necrosis factor | Proteomics | Skin | Autoimmune diseases | Index Medicus
Journal Article
Autophagy, ISSN 1554-8635, 05/2015, Volume 11, Issue 5, pp. 729 - 739
... to a variety of stress stimuli, including nutrient or growth factor deprivation, hypoxia, reactive oxygen species (ROS), DNA damage, protein aggregates, damaged organelles... 
ATF4, activating transcription factor 4 | HIF1A, hypoxia inducible factor 1, α subunit (basic helix-loop-helix transcription factor) | HDAC3, histone deacetylase 3 | XPO1, exportin 1 | EGF, epidermal growth factor | MAP1LC3A, microtubule-associated protein 1 light chain 3 α | LMP, lysosomal membrane permeabilization | COX8, cytochrome c oxidase subunit VIII | MMP14, matrix metallopeptidase 14 (membrane-inserted) | MLS, mitochondrial localization sequence | EIF2AK2, eukaryotic translation initiation factor 2-α kinase 2 | CuB, cucurbitacin B | autophagy | IMM, inner mitochondrial membrane | CTSL, cathepsin L | IL6, interleukin 6 | miRNA, microRNA | CTSB, cathepsin B | PDGFRB, platelet-derived growth factor receptor, β polypeptide | receptor tyrosine kinases | RTK, receptor tyrosine kinases | PTPN2, protein tyrosine phosphatase, non-receptor type 2 | CNTF, ciliary neurotrophic factor | MAPK1, mitogen-activated protein kinase 1 | ALK, anaplastic lymphoma receptor tyrosine kinase | NES, nuclear export signal | EIF2A, eukaryotic initiation factor 2A, 65kDa | NDUFA13, NADH dehydrogenase (ubiquinone) 1 α subcomplex, 13 | VHL, von Hippel-Lindau tumor suppressor, E3 ubiquitin protein ligase | PTPN6, protein tyrosine phosphatase, non-receptor type 6 | ROS, reactive oxygen species | ETC, electron transport chain | SH2, src homology 2 | targeted therapy | PRKAA2, protein kinase, AMP-activated, α 2 catalytic subunit | STAT3 | BNIP3, BCL2/adenovirus E1B 19kDa interacting protein 3 | NFKB1, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 | STAT3, signal transducer and activator of transcription 3 (acute-phase response factor) | NLS, nuclear localization signal | FOXO1/3, forkhead box O1/3 | mitoSTAT3, mitochondrial STAT3 | mitophagy | PTPN11, protein tyrosine phosphatase, non-receptor type 11 | KDR, kinase insert domain receptor | cancer | ConA, concanavalin A | CYCS, cytochrome c, somatic | ER, endoplasmic reticulum | Mitophagy | Targeted therapy | Autophagy | Receptor tyrosine kinases | Cancer | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Neoplasms - metabolism | Neoplasms - therapy | Animals | Models, Biological | Humans | Mitochondria - metabolism | STAT3 Transcription Factor - chemistry | Subcellular Fractions - metabolism | STAT3 Transcription Factor - metabolism | Index Medicus
Journal Article
PloS one, ISSN 1932-6203, 10/2012, Volume 7, Issue 10, pp. e46082 - e46082
.... It also induced the release of interleukin (IL)-17A by Th17 cells, but not the release of IL-10 and transforming growth factor (TGF... 
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | GATA3 Transcription Factor - genetics | T-Lymphocytes, Regulatory - metabolism | Transforming Growth Factor beta1 - metabolism | STAT Transcription Factors - metabolism | Suppressor of Cytokine Signaling 1 Protein | Janus Kinases - metabolism | Interferon-gamma - metabolism | Cell Differentiation - genetics | Th17 Cells - metabolism | Base Sequence | T-Lymphocytes, Regulatory - cytology | Interleukin-10 - metabolism | Th17 Cells - cytology | Interferon-gamma - genetics | Interleukin-4 - genetics | GATA3 Transcription Factor - metabolism | Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics | Signal Transduction | Interleukin-4 - metabolism | Gene Expression Regulation | Suppressor of Cytokine Signaling Proteins - genetics | Forkhead Transcription Factors - genetics | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Interleukin-17 - metabolism | Animals | Mice | MicroRNAs - genetics | Smad Proteins - metabolism | Physiological aspects | Genetic aspects | MicroRNA | Research | Cell differentiation | T cells | Smad5 protein | Smad protein | Transcription factors | Transcription | Laboratories | Interleukin | Differentiation (biology) | Helper cells | Science | Homology | Lymphocytes T | Inflammatory diseases | Signal transduction | Immunology | Transfection | Lymphocytes | Smad2 protein | Atherosclerosis | CD25 antigen | Janus kinase | miRNA | Cardiology | Growth factors | Immune system | Function analysis | Lupus | Immune response | Cytokines | Cell lineage | T cell receptors | Gene expression | Ribonucleic acid--RNA | Suppressors | CD4 antigen | Signaling | MicroRNAs | Interleukin 10 | Index Medicus | RNA | Ribonucleic acid
Journal Article
Immunity (Cambridge, Mass.), ISSN 1074-7613, 04/2018, Volume 48, Issue 4, pp. 659 - 674.e6
Journal Article
10.