W A Border

Summary

Affiliation: University of Utah
Country: USA

Publications

  1. ncbi request reprint Interactions of transforming growth factor-beta and angiotensin II in renal fibrosis
    W A Border
    Department of Medicine, University of Utah Health Sciences Center, Salt Lake City, 84132, USA
    Hypertension 31:181-8. 1998
  2. ncbi request reprint t-PA promotes glomerular plasmin generation and matrix degradation in experimental glomerulonephritis
    M Haraguchi
    Fibrosis Research Laboratory, Division of Nephrology, University of Utah, Salt Lake City, Utah 84108, USA
    Kidney Int 59:2146-55. 2001
  3. ncbi request reprint Maximizing hemodynamic-independent effects of angiotensin II antagonists in fibrotic diseases
    W A Border
    Fibrosis Research Laboratory, University of Utah School of Medicine, Salt Lake City, UT 84108, USA
    Semin Nephrol 21:563-72. 2001
  4. ncbi request reprint Noninhibitory PAI-1 enhances plasmin-mediated matrix degradation both in vitro and in experimental nephritis
    Y 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
  5. ncbi request reprint Renin-stimulated TGF-beta1 expression is regulated by a mitogen-activated protein kinase in mesangial cells
    Y Huang
    Division of Nephrology, Fibrosis Research Laboratory, University of Utah, Salt Lake City, Utah 84108, USA
    Kidney Int 72:45-52. 2007
  6. ncbi request reprint Perspectives on blockade of TGFbeta overexpression
    Y Huang
    Fibrosis Research Laboratory, Division of Nephrology, University of Utah School of Medicine, Salt Lake City, 84108, USA
    Kidney Int 69:1713-4. 2006
  7. ncbi request reprint Increased levels of transforming growth factor-beta in HIV-associated nephropathy
    T Yamamoto
    Division of Nephrology and Hypertension, University of Utah School of Medicine, Salt Lake City, USA
    Kidney Int 55:579-92. 1999

Collaborators

Detail Information

Publications7

  1. ncbi request reprint Interactions of transforming growth factor-beta and angiotensin II in renal fibrosis
    W 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...
  2. ncbi request reprint t-PA promotes glomerular plasmin generation and matrix degradation in experimental glomerulonephritis
    M 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...
  3. ncbi request reprint Maximizing hemodynamic-independent effects of angiotensin II antagonists in fibrotic diseases
    W 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...
  4. ncbi request reprint Noninhibitory PAI-1 enhances plasmin-mediated matrix degradation both in vitro and in experimental nephritis
    Y 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...
  5. ncbi request reprint Renin-stimulated TGF-beta1 expression is regulated by a mitogen-activated protein kinase in mesangial cells
    Y 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...
  6. ncbi request reprint Perspectives on blockade of TGFbeta overexpression
    Y 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...
  7. ncbi request reprint Increased levels of transforming growth factor-beta in HIV-associated nephropathy
    T 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...