Disruption of Smad7 promotes ANG II-mediated renal inflammation and fibrosis via Sp1-TGF-β/Smad3-NF.κB-dependent mechanisms in mice
| Autor: | You-Qi Li, Rainer Heuchel, Hai-Yong Chen, Yong-Jun Shi, Guan-Xian Liu, Xiao-Ru Huang, Hui-Yao Lan, Lihua Wei |
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| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Male
Anatomy and Physiology Mouse Kidney Cardiovascular Mice Transforming Growth Factor beta Fibrosis Medicine Mice Knockout Multidisciplinary integumentary system Angiotensin II NF-kappa B Animal Models Hypertensive kidney disease Proteinuria medicine.anatomical_structure Nephrology Hypertension Kidney Diseases medicine.symptom Signal Transduction Research Article medicine.medical_specialty Sp1 Transcription Factor Science Inflammation Smad7 Protein Model Organisms Internal medicine Hypertensive Nephropathy Genetics Renal fibrosis Animals Smad3 Protein Biology Renal Physiology business.industry Immunity Kidney metabolism Renal System medicine.disease MicroRNAs Endocrinology Gene Expression Regulation Clinical Immunology Gene Function business |
| Zdroj: | PLoS ONE, Vol 8, Iss 1, p e53573 (2013) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | Smad7 is an inhibitory Smad and plays a protective role in obstructive and diabetic kidney disease. However, the role and mechanisms of Smad7 in hypertensive nephropathy remains unexplored. Thus, the aim of this study was to investigate the role and regulatory mechanisms of Smad7 in ANG II-induced hypertensive nephropathy. Smad7 gene knockout (KO) and wild-type (WT) mice received a subcutaneous infusion of ANG II or control saline for 4 weeks via osmotic mini-pumps. ANG II infusion produced equivalent hypertension in Smad7 KO and WT mice; however, Smad7 KO mice exhibited more severe renal functional injury as shown by increased proteinuria and reduced renal function (both p published_or_final_version |
| Databáze: | OpenAIRE |
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