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Renal fibrosis: Role of impaired protein degradation and potential therapeutic strategies

Heidland A.1, Sebekova K.2, Paczek L.3, Teschner M.1, Daemmrich J.4, Gaciong Z.3

1 Medical Faculty, University of Wuerzburg, 2 Institute of Preventive and Clinical Medicine, Bratislava (Slovakia), 3 The Transplantation Institute Warsaw (Poland), 4 Institute of Pathology, University of Wuerzburg (Germany)

Kidney International 1997, Vol. 52, Suppl. 62,  pp. S 32- S 35 

343 KA (5-08-3)
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Cellular protein content and extracellular matrix (ECM) components represent a dynamic balance between synthesis and degradation. In glomerulosclerosis and tubulointerstitial fibrosis this balance is disrupted: Upregulation of protein synthesis and/or downregulation of proteolytic enzymes cause cellular hypertrophy and expansion of ECM (Baricos 1994). On the contrary in inflammatory renal diseases enhanced proteolytic activities (from invading blood cells or resident cells) damage glomerular basement membrane (GBM) components (with subsequent proteinuria) and/or non-GBM proteins (resulting in mesangiolysis, Baricos and Shah 1991 ).

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