Endothelin is a key modulator of progressive renal injury: Experimental data and novel therapeutic strategies

Isabella Bruzzi, Ariela Benigni

Research output: Contribution to journalArticle

Abstract

Glomerulosclerosis and tubulointerstitial damage are common histological abnormalities of many renal diseases that progress to end-stage renal failure. In some models of renal damage, glomerulosclerosis seems to be associated with increased glomerular capillary pressure. Due to the positive correlation of glomerulosclerosis and proteinuria in both experimental models and in humans, abnormal permeability to macromolecules has also been considered a possible determinant of glomerulosclerosis. Abnormally filtered macromolecules have an intrinsic toxicity to the kidney due to protein over-reabsorption, possibly leading to tubulointerstitial damage. Endothelin-1 (ET-1) is a vasoconstrictor peptide that induces mitogenesis and the accumulation of matrix proteins by mesangial cells. Evidence is available that ET-1 plays a role in progressive renal disease in different experimental models, including renal mass reduction, lupus nephritis, streptozotocin-induced diabetes and puromycin-induced nephrosis.

Original languageEnglish
Pages (from-to)349-353
Number of pages5
JournalClinical and Experimental Pharmacology and Physiology
Volume23
Issue number4
Publication statusPublished - 1996

Keywords

  • endothelin
  • endothelin-receptor antagonist
  • glomerulosclerosis
  • renal mass ablation
  • tubulo-interstitial damage

ASJC Scopus subject areas

  • Physiology
  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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