TY - JOUR
T1 - Section review
T2 - Cardiovascular & renal: Inhibition of macrophage function as a potential therapeutic strategy for the treatment of renal disease
AU - Van Goor, Harry
AU - Diamond, Jonathan R.
AU - Elema, Job D.
AU - Ricardo, Sharon D.
PY - 1995/11/1
Y1 - 1995/11/1
N2 - A variety of human renal diseases are associated with the glomerular and tubular accumulation of bone marrow-derived monocyte/macrophages. In addition, seminal evidence has been provided for the crucial contribution of macrophages to the progression of renal disease in laboratory animals. At present, not all mechanisms by which macrophages enter the renal interstitium and glomerular mesangium have been elucidated. Furthermore, we are still uncertain as to whether macrophages release cytokines, growth factors and other mediators (such as prostaglandins, bioactive lipids, and nitric oxide) simultaneously or in a more selective, regulated manner, i.e., one in which the cells release some, but not all, of their products. It is the purpose of this paper to describe the mechanisms whereby macrophages are recruited to the kidney, their possible involvement in renal deterioration, and possible therapeutic strategies for preventing the recruitment of renal macrophages and/or suppiessing the fibrogenic and inflammatory ability of this pluripotential inflammatory cell. 1995
AB - A variety of human renal diseases are associated with the glomerular and tubular accumulation of bone marrow-derived monocyte/macrophages. In addition, seminal evidence has been provided for the crucial contribution of macrophages to the progression of renal disease in laboratory animals. At present, not all mechanisms by which macrophages enter the renal interstitium and glomerular mesangium have been elucidated. Furthermore, we are still uncertain as to whether macrophages release cytokines, growth factors and other mediators (such as prostaglandins, bioactive lipids, and nitric oxide) simultaneously or in a more selective, regulated manner, i.e., one in which the cells release some, but not all, of their products. It is the purpose of this paper to describe the mechanisms whereby macrophages are recruited to the kidney, their possible involvement in renal deterioration, and possible therapeutic strategies for preventing the recruitment of renal macrophages and/or suppiessing the fibrogenic and inflammatory ability of this pluripotential inflammatory cell. 1995
UR - http://www.scopus.com/inward/record.url?scp=0028865338&partnerID=8YFLogxK
U2 - 10.1517/13543784.4.11.1151
DO - 10.1517/13543784.4.11.1151
M3 - Article
AN - SCOPUS:0028865338
SN - 1354-3784
VL - 4
SP - 1151
EP - 1159
JO - Expert Opinion on Investigational Drugs
JF - Expert Opinion on Investigational Drugs
IS - 11
ER -