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©2012 Baishideng Publishing Group Co.
World J Diabetes. Jan 15, 2012; 3(1): 7-18
Published online Jan 15, 2012. doi: 10.4239/wjd.v3.i1.7
Published online Jan 15, 2012. doi: 10.4239/wjd.v3.i1.7
Increase expression and synthesis of chemokines, adhesion molecules, transcription factors, cytokines, growth factors and mediators of inflammation |
Alteration of synthesis of prostaglandins and hyaluronan |
Stimulation of oxidative stress |
Induction of intraglomerular hemodynamic abnormalities |
Increase of vascular endothelial cell permeability |
Induction of cell proliferation and contraction, and inhibition of endothelium relaxation |
Increase fibronectin expression |
Induction of cell apoptosis and necrosis |
Induction of glomerular hypertrophy |
Stimulation of plasminogen activator inhibitor-1 production |
Reduction of tissue factor inhibitor and thrombomodulin expression |
Stimulation of inflammatory cells recruitment and activation |
Induction of major histocompatibility complex antigen expression |
- Citation: Luis-Rodríguez D, Martínez-Castelao A, Górriz JL, Álvaro F, Navarro-González JF. Pathophysiological role and therapeutic implications of inflammation in diabetic nephropathy. World J Diabetes 2012; 3(1): 7-18
- URL: https://www.wjgnet.com/1948-9358/full/v3/i1/7.htm
- DOI: https://dx.doi.org/10.4239/wjd.v3.i1.7