Transformation of interstitial fibroblasts and tubulointerstitial fibrosis in diabetic nephropathy

被引：73

作者：

Ina K. ^{[2
]}

Kitamura H. ^{[2
]}

Tatsukawa S. ^{[2
]}

Takayama T. ^{[2
]}

Fujikura Y. ^{[2
]}

Shimada T. ^{[1
]}

机构：

[1] Department of Health Sciences, School of Nursing, Oita Medical University, Oita

[2] Department of Anatomy, Oita Medical University, Oita 879-5593, 1-1 Idaigaoka, Hasama-machi

来源：

Medical Electron Microscopy | 2002年 / 35卷 / 2期

关键词：

Diabetic nephropathy; Myofibroblast; Transforming growth factor (TGF)-β; Tubulointerstitial fibrosis;

D O I：

10.1007/s007950200011

中图分类号：

学科分类号：

摘要：

The developmental mechanism of tubulointerstitial fibrosis in diabetic nephropathy (DN) has not been elucidated. Tubulointerstitial fibrosis, as well as glomerulosclerosis, occurs in DN. Myofibroblasts which overproduce extracellular matrix are present in the renal interstitium in diabetics, although they are almost never seen in normal kidneys. The myofibroblasts appear to originate from interstitial fibroblasts. In addition, transforming growth factor-β1 (TGF-β1), which can evoke myofibroblast transformation, is detected in interstitial cells in the diabetic kidney, but not in the normal kidney. Taken together, these findings led us to speculate that TGF-β1 induces the transformation of interstitial fibroblasts into myofibroblasts, followed by tubulointerstitial fibrosis. Based on this speculation, we discuss the developmental mechanism of tubulointerstitial fibrosis in this review.

引用

页码：87 / 95

页数：8

共 67 条

[1]

Bohle A., Glomb D., Grund K.E., Mackensen S., Correlations between relative interstitial volume of the renal cortex and serum creatinine concentration in minimal changes with nephritic syndrome and in focal sclerosing glomerulonephritis, Virchows Arch A Pathol Anat Histopathol, 376, pp. 221-232, (1977)

[2]

Bohle A., Grund K.E., Mackensen S., Tolon M., Correlations between renal interstitium and level of serum creatinine. Morphometric investigations of biopsies in perimembranous glomerulonephritis, Virchows Arch A Pathol Anat Histopathol, 373, pp. 15-22, (1977)

[3]

Bohle A., Bader R., Grund K.E., Mackensen S., Neunhoeffer J., Serum creatinine concentration and renal interstitial volume. Analysis of correlations in endocapillary (acute) glomerulonephritis and in moderately severe mesangioproliferative glomerulonephritis, Virchows Arch A Pathol Anat Histopathol, 375, pp. 87-96, (1977)

[4]

Schwartz M.M., Fennell J.S., Lewis E.J., Pathologic changes in the renal tubule in systemic lupus erythematosus, Hum Pathol, 13, pp. 534-547, (1982)

[5]

Wehrmann M., Bohle A., Bogenschutz O., Eissele R., Freislederer A., Ohlschlegel C., Schumm G., Batz C., Gartner H.-V., Long-term prognosis of chronic idiopathic membranous glomerulonephritis. An analysis of 334 cases with particular regard to tubulo-interstitial changes, Clin Nephrol, 31, pp. 67-76, (1989)

[6]

Alexopoulos E., Seron D., Hartley R.B., Cameron J.S., Lupus nephritis: Correlation of interstitial cells with glomerular function, Kidney Int, 37, pp. 100-109, (1990)

[7]

Bohle A., Wehrmann M., Bogenschutz O., Batz C., Muller G.A., The pathogenesis of chronic renal failure in diabetic nephropathy, Pathol Res Pract, 187, pp. 251-259, (1991)

[8]

Lane P.H., Steffes M.W., Fioretto P., Mauer S.M., Renal interstitial expansion in insulin-dependent diabetes mellitus, Kidney Int, 43, pp. 661-667, (1993)

[9]

Moriya T., Tanaka K., Moriya R., Glomerular structural changes and structural-functional relationships at early stage of diabetic nephropathy in Japanese type 2 diabetic patients, Med Electron Microsc, 33, pp. 115-122, (2000)

[10]

Isogai S., Mogami K., Ouchi H., Yoshino G., An impairment of barrier size and charge selectivity of glomerular basement membrane in streptozotocin-induced diabetes and prevention by pharmacological therapy, Med Electron Microsc, 33, pp. 123-129, (2000)

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