Abstract
GLOMERULONEPHRITIS is an inflammation of the kidney characterized by the accumulation of extracellular matrix within the damaged glomeruli1–4, impaired filtration and proteinuria. In its progressive form, the disease destroys kidney function leading to uraemia and death, unless dialysis therapy or kidney transplantation is available. The pathogenesis of glomerulonephritis is incompletely understood, but the eliciting factor is thought often to be an immunological injury to mesangial and/or other resident cells in the glomeruli5,6. We have used an animal model of acute mesangial proliferative glomerulonephritis7,8 to show that this disease is associated with increased production and activity of transforming growth factor β1 (TGF-βl)9, an inducer of extracellular matrix production10–17. Here we report that administration of anti-TGF-βl at the time of induction of the glomerular disease suppresses the increased production of extracellular matrix and dramatically attenuates histological manifestations of the disease. These results provide direct evidence for a causal role of TGF-βl in the pathogenesis of the experimental disease and suggest a new approach to the therapy of glomerulonephritis.
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Border, W., Okuda, S., Languino, L. et al. Suppression of experimental glomerulonephritis by antiserum against transforming growth factor β1. Nature 346, 371–374 (1990). https://doi.org/10.1038/346371a0
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DOI: https://doi.org/10.1038/346371a0
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