Table 1 Summary effects of different molecules involved in inflammation in the obstructive nephropathy
From: Role of inflammation in túbulo-interstitial damage associated to obstructive nephropathy
Agent | Effect |
|---|---|
NF-κB | Inflammatory gene expression Macrophage infiltration Renal tubular cell apoptosis |
Ang II | NF-κB activation Oxidative stress TGF-β upregulation Macrophage infiltration |
TNF-α | Macrophage infiltration Renal tubular cell death |
IL-1 | ICAM expression Macrophage infiltration Fibroblast activation |
MIF | Leukocyte activation Fibroblast proliferation |
E,P,L Selectins | Monocytes/macrophage and T cell infiltration Tubular apoptosis |
VCAM, ICAM | Interstitial inflammation Leukocyte infiltration |
β-integrins | Macrophage infiltration |
MCP-1, RANTES, MIP-1α | Macrophage recruitment |
CCR1, CCR2 | Leukocyte recruitment Interstitial fibrosis |
JAMS | Leukocyte recruitment |
M-CSF | Macrophage infiltration, activation and proliferation Tubular apoptosis |
IP-10 | Leukocyte recruitment |
TGF-β | Monocyte/macrophage infiltration Fibroblast proliferation Tubular apoptosis |
HGF | Suppress macrophage infiltration Inhibit chemokine expression |
OPN | Macrophage infiltration Interstitial fibrosis Repress tubular cell apoptosis |
iNOS | Resistance to cell death Limit macrophage infiltration |