Ablation of aryl hydrocarbon receptor promotes angiotensin II-induced cardiac fibrosis through enhanced c-Jun/HIF-1α signaling - Ichihara, Sahoko; Li, Ping; Mise, Nathan; Suzuki, Yuka; Izuoka, Kiyora; Nakajima, Tamie; Gonzalez, Frank; Ichihara, Gaku (Archives of toxicology, 2019)
Keywords: Ablation; AhR gene; Angiotensin; Angiotensin II; Angiotensin II - toxicity; Animals; Aromatic compounds; Aromatic hydrocarbons; Basic Helix-Loop-Helix Transcription Factors - genetics; Basic Helix-Loop-Helix Transcription Factors - metabolism; Biomedical and Life Sciences; Biomedicine; Blood pressure; Blood Pressure - drug effects; c-Jun protein; Deoxyribonucleic acid; DNA; Endothelins; Environmental Health; Fenofibrate; Fenofibrate - pharmacology; Fibrosis; Growth factors; Halogenated hydrocarbons; Heart; Hydrocarbons; Hypertrophy; Hypertrophy, Left Ventricular - pathology; Hypoxia; Hypoxia-Inducible Factor 1, alpha Subunit - genetics; Hypoxia-inducible factors; JNK Mitogen-Activated Protein Kinases - genetics; Ligands; Male; Mice; Mice, Knockout; Molecular Toxicology; Myocardium - pathology; Occupational Medicine/Industrial Medicine; Pharmacology/Toxicology; PPAR alpha - agonists; Receptors, Aryl Hydrocarbon - genetics; Receptors, Aryl Hydrocarbon - metabolism; Rodents; Signal transduction; Signal Transduction - drug effects; Signal Transduction - genetics; Signaling; Transcription factors; Vascular endothelial growth factor; Vascular Endothelial Growth Factor A - biosynthesis; Vascular Endothelial Growth Factor A - genetics; Ventricle; Xenobiotics; Fibrosis; Cardiac hypertrophy; HIF-1α; AHR; Angiotensin II; PPARα; Vascular endothelial growth factor