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. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: Am J Kidney Dis. 2011 Jan 15;57(3):498–507. doi: 10.1053/j.ajkd.2010.10.052

Table 3.

Potential therapeutic targets/pathways for modulation of pathogenic glomerular responses in glomerular diseases

MODEL Target Agent Therapeutic effect in
kidney
Reference
Thy1.1 induced GN EGR1 Antisense ODN reduced mesangial cell proliferation 49
E2F Decoy ODN reduced PCNA and cdk2 kinase 50
AP1 Decoy ODN reduced TGFβ, PAI, mesangial cell proliferation, ECM production 51
MAPK1 siRNA Reduced TGFβ, glomerulosclerosis, PAI, ECM production 52
anti-GBM nephritis NFκB Decoy ODN Reduced IL-1β, ICAM, inflammation, proteinuria 53
Anti-E selectin immunoliposomes dexamethasone Reduced ICAM, inflammation 54,55
Streptozotocin induced diabetic nephropathy TGFβ Antisense ODN Reduced TGFβ in urine and kidney 56
SP1 Decoy ODN Reduced type IV collagen, fibronectin, α-smooth muscle actin 57

Abbreviations: cdk2, cyclin dependent kinase 2; ODN, oligodeoxynucleotide; PCNA, proliferating cell nuclear antigen; EGR1, early growth response 1; GN, glomerulonephritis; siRNA, small interfering RNA; TGFβ, transforming growth factor β; GBM, glomerular basement membrane; IV, intravenous; ECM, extracellular matrix; NFκB, nuclear factor-κB; MAPK, mitogen-activated protein kinase; PAI, plasminogen activator inhibitor; IL-1β, interleukin 1β.