Advanced Glomerulosclerosis Is Reversible in Nephrotic Mice

Advanced glomerulosclerosis, a common hallmark of chronic renal diseases (CRD) is believed to be irreversible, and it is thought that glomerular hyperfiltration and hypertrophy may participate in its pathogenesis. We demonstrate here that glomerulosclerosis is “reversible” in an animal model. We use...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2001-06, Vol.284 (3), p.707-713
Main Authors: Mizuno-Horikawa, Yoko, Mizuno, Shinya, Tamura, Shinichi, Kurosawa, Tsutomu
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Fibroblasts
Fibronectins - metabolism
glomerular hypertrophy
glomerular remodeling
glomerulosclerosis
Glomerulosclerosis, Focal Segmental - metabolism
Glomerulosclerosis, Focal Segmental - pathology
Glomerulosclerosis, Focal Segmental - therapy
Hypertrophy - pathology
Hypertrophy - therapy
Kidney Failure, Chronic - metabolism
Kidney Failure, Chronic - pathology
Kidney Failure, Chronic - therapy
Kidney Glomerulus - cytology
Kidney Glomerulus - metabolism
Kidney Glomerulus - pathology
Ligation
Mice
Mice, Mutant Strains
mouse model
myofibroblasts
nephrotic syndrome
Sclerosis
Ureter
ureter ligation
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Summary:Advanced glomerulosclerosis, a common hallmark of chronic renal diseases (CRD) is believed to be irreversible, and it is thought that glomerular hyperfiltration and hypertrophy may participate in its pathogenesis. We demonstrate here that glomerulosclerosis is “reversible” in an animal model. We used nephrotic ICGN (nep/nep) mice which showed a rapid progression of glomerulosclerosis, accompanied by histological findings for glomerular hyperfiltration. It is known that ureter ligation reduces glomerular filtration in ligated kidneys. When ureter ligation was applied to our model, glomerulosclerosis (characterized by myofibroblast hyperplasia and over-accumulated matrix protein) weakened in conjunction with suppressed glomerular hypertrophy. During this process, glomerular myofibroblasts showed apoptotic cell death after unilateral ureter ligation (UUO) treatment. Our results suggest that inhibition of glomerular filtration in sclerotic tufts may cause glomerular remodeling through the modulation of molecular and cellular sclerogenesis.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.2001.4903