scholarly journals Inhibition of tumor necrosis factor signaling attenuates renal immune cell infiltration in experimental membranous nephropathy

Oncotarget ◽  
2017 ◽  
Vol 8 (67) ◽  
pp. 111631-111641 ◽  
Author(s):  
Yen-Sung Huang ◽  
Shin-Huei Fu ◽  
Kuo-Cheng Lu ◽  
Jin-Shuen Chen ◽  
Hsin-Yi Hsieh ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Membranous Nephropathy ◽  
Tumor Necrosis ◽  
Immune Cell ◽  
Cell Infiltration ◽  
Immune Cell Infiltration ◽  
Tumor Necrosis Factor Signaling ◽  
Necrosis Factor

scholarly journals A trigger model of apoptosis induced by tumor necrosis factor signaling

2011 ◽  
Vol 5 (Suppl 1) ◽  
pp. S13 ◽  
Author(s):  
Chang Gu ◽  
Junjie Zhang ◽  
Yingyu Chen ◽  
Jinzhi Lei
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Signaling ◽  
Necrosis Factor

scholarly journals Blockade of Tumor Necrosis Factor   Signaling in Tumor-Associated Macrophages as a Radiosensitizing Strategy

2010 ◽  
Vol 70 (4) ◽  
pp. 1534-1543 ◽  
Author(s):  
Y. Meng ◽  
M. A. Beckett ◽  
H. Liang ◽  
H. J. Mauceri ◽  
N. van Rooijen ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Associated Macrophages ◽  
Tumor Necrosis Factor Signaling ◽  
Necrosis Factor

Functional dichotomy of neutral and acidic sphingomyelinases in tumor necrosis factor signaling

Cell ◽  
1994 ◽  
Vol 78 (6) ◽  
pp. 1005-1015 ◽  
Author(s):  
Katja Wiegmann ◽  
Stefan Schütze ◽  
Thomas Machleidt ◽  
Dorothee Witte ◽  
Martin Krönke
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Signaling ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor-α: regulation of renal function and blood pressure

2013 ◽  
Vol 304 (10) ◽  
pp. F1231-F1242 ◽  
Author(s):  
Vanesa D. Ramseyer ◽  
Jeffrey L. Garvin
Keyword(s):  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Immune Cell ◽  
Organ Damage ◽  
Physiological Status ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine that becomes elevated in chronic inflammatory states such as hypertension and diabetes and has been found to mediate both increases and decreases in blood pressure. High levels of TNF-α decrease blood pressure, whereas moderate increases in TNF-α have been associated with increased NaCl retention and hypertension. The explanation for these disparate effects is not clear but could simply be due to different concentrations of TNF-α within the kidney, the physiological status of the subject, or the type of stimulus initiating the inflammatory response. TNF-α alters renal hemodynamics and nephron transport, affecting both activity and expression of transporters. It also mediates organ damage by stimulating immune cell infiltration and cell death. Here we will summarize the available findings and attempt to provide plausible explanations for such discrepancies.

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