W A Border
Affiliation: University of Utah
- Interactions of transforming growth factor-beta and angiotensin II in renal fibrosisW A Border
Department of Medicine, University of Utah Health Sciences Center, Salt Lake City, 84132, USA
Hypertension 31:181-8. 1998..Higher doses or different combinations of drugs that block the renin-angiotensin system or entirely new drug strategies may be needed to achieve a greater antifibrotic effect...
- t-PA promotes glomerular plasmin generation and matrix degradation in experimental glomerulonephritisM Haraguchi
Fibrosis Research Laboratory, Division of Nephrology, University of Utah, Salt Lake City, Utah 84108, USA
Kidney Int 59:2146-55. 2001..Agents that increase plasmin generation, such as t-PA, may have potential as antifibrotic therapies...
- Maximizing hemodynamic-independent effects of angiotensin II antagonists in fibrotic diseasesW A Border
Fibrosis Research Laboratory, University of Utah School of Medicine, Salt Lake City, UT 84108, USA
Semin Nephrol 21:563-72. 2001..However, it further suggests that higher doses and/or a combination of angiotensin II blockade with another agent or agents might truly halt progressive fibrosis...
- Noninhibitory PAI-1 enhances plasmin-mediated matrix degradation both in vitro and in experimental nephritisY Huang
Fibrosis Research Laboratory, Division of Nephrology, University of Utah School of Medicine, Salt Lake City, Utah 84108, USA
Kidney Int 70:515-22. 2006..PAI-1R reduces pathological ECM accumulation, in large part through effectively competing with native PAI-1 thereby restoring plasmin generation and increasing plasmin-dependent degradation of matrix components...
- Renin-stimulated TGF-beta1 expression is regulated by a mitogen-activated protein kinase in mesangial cellsY Huang
Division of Nephrology, Fibrosis Research Laboratory, University of Utah, Salt Lake City, Utah 84108, USA
Kidney Int 72:45-52. 2007..This renin-activated pathway triggers cell proliferation along with TGF-beta1 and plasminogen activator inhibitor-1 gene expression. This system may play an important role in the overall profibrotic actions of renin...
- Perspectives on blockade of TGFbeta overexpressionY Huang
Fibrosis Research Laboratory, Division of Nephrology, University of Utah School of Medicine, Salt Lake City, 84108, USA
Kidney Int 69:1713-4. 2006..using the unilateral ureteral obstruction model, provide a new target for therapeutic intervention by identifying loss of the Smad corepressors Ski and SnoN as a mechanism that amplifies the profibrotic actions of TGFbeta...
- Increased levels of transforming growth factor-beta in HIV-associated nephropathyT Yamamoto
Division of Nephrology and Hypertension, University of Utah School of Medicine, Salt Lake City, USA
Kidney Int 55:579-92. 1999..Recent evidence suggests that the fibrogenic cytokine transforming growth factor-beta (TGF-beta) might be involved. We hypothesized that overproduction of TGF-beta in the kidney might be involved in the pathogenesis of HIVAN...