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Nephrol Dial Transplant (1999) 14: 2551-2553
© 1999 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Novel approaches to unravel the genesis of glomerulosclerosis by new methodologies in molecular biology and molecular genetics

Jun Wada, Kenich Shikata and Hirofumi Makino

Okayama University Medical School, Department of Medicine III, Okayama, Japan

Correspondence and offprint requests to: Hirofumi Makino, MD, Professor and Chairman, Department of Medicine III, Okayama University Medical School, 2–5-1 Shikata-cho, Okayama 700– 8558, Japan.

Introduction

Glomerulosclerosis is the common pathological feature in most immunological and non-immunological renal diseases and tightly related to the progression of renal failure. Although numerous attempts have been made to elucidate its mechanism, the precise pathogenesis of glomerulosclerosis still remains to be investigated. In morphological studies, glomerulosclerosis is characterized by the depletion of glomerular cells and the accumulation of extracellular matrix, including type I, III and IV collagen, fibronectin, laminin and proteoglycans [1]. Since transforming growth factor-ß (TGF-ß) is implicated in the regulation of production and degradation of matrix glycoproteins, the role of TGF-ß was investigated extensively and has been well documented. These studies indicated that the mesangial cell-derived TGF-ß is stimulated by immunological and non-immunological insults and is responsible for glomerulosclerosis by directly stimulating the synthesis of extracellular matrix (ECM) glycoproteins and reducing collagenase production. In glomerulonephritis, the pathological immune reactions induce the . . . [Full Text of this Article]

Gene expression profile in normal, developmental and pathological states of the kidney

Functional studies using knockout and transgenic animals

Approach to glomerulosclerosis-related genes using molecular genetics

Conclusions

References


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