Endothelin-1 is identified as a key modulator of progressive renal injury in experimental models, highlighting it as a potential target for novel therapeutic strategies.
Endothelin-1 remains a preclinical target in renal disease; leaves open whether inhibition slows progression in patients.
Glomerulosclerosis and tubulointerstitial damage are common histological abnormalities of many renal diseases that progress to end-stage renal failure. 2. In some models of renal damage, glomerulosclerosis seems to be associated with increased glomerular capillary pressure. 3. 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. 4. Abnormally filtered macromolecules have an intrinsic toxicity to the kidney due to protein over-reabsorption, possibly leading to tubulointerstitial damage. 5. Endothelin-1 (ET-1) is a vasoconstrictor peptide that induces mitogenesis and the accumulation of matrix proteins by mesangial cells. 6. 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.
No takes yet. Share an insight, caveat, or question.
Bruzzi et al. (1996) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: