G H Tesch

Summary

Affiliation: Monash University
Country: Australia

Publications

  1. ncbi Role of macrophages in complications of type 2 diabetes
    G H Tesch
    Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Clin Exp Pharmacol Physiol 34:1016-9. 2007
  2. ncbi Review: Serum and urine biomarkers of kidney disease: A pathophysiological perspective
    Greg H Tesch
    Department of Nephrology, Monash University, Monash Medical Centre, Clayton, Victoria, Australia
    Nephrology (Carlton) 15:609-16. 2010
  3. ncbi Macrophages and diabetic nephropathy
    Greg H Tesch
    Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Semin Nephrol 30:290-301. 2010
  4. ncbi MCP-1/CCL2: a new diagnostic marker and therapeutic target for progressive renal injury in diabetic nephropathy
    G H Tesch
    Dept of Nephrology, Monash Medical Centre, 246 Clayton Rd, Clayton, Victoria 3168, Australia
    Am J Physiol Renal Physiol 294:F697-701. 2008
  5. ncbi Rodent models of streptozotocin-induced diabetic nephropathy
    Greg H Tesch
    Department of Nephrology, Monash University, Monash Medical Centre, Clayton, Victoria, Australia
    Nephrology (Carlton) 12:261-6. 2007
  6. ncbi Role of MKK3-p38 MAPK signalling in the development of type 2 diabetes and renal injury in obese db/db mice
    A K H Lim
    Department of Nephrology, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia
    Diabetologia 52:347-58. 2009
  7. ncbi Lymphocytes promote albuminuria, but not renal dysfunction or histological damage in a mouse model of diabetic renal injury
    A K H Lim
    Department of Nephrology, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia
    Diabetologia 53:1772-82. 2010
  8. ncbi Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice
    F Y Chow
    Department of Nephrology, Monash Medical Centre, Clayton, Vic, 3168, Australia
    Diabetologia 50:471-80. 2007
  9. ncbi Monocyte chemoattractant protein-1 promotes the development of diabetic renal injury in streptozotocin-treated mice
    F Y Chow
    Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 69:73-80. 2006
  10. ncbi Antibody blockade of c-fms suppresses the progression of inflammation and injury in early diabetic nephropathy in obese db/db mice
    A K H Lim
    Department of Nephrology, Monash Medical Centre, Clayton, Victoria 3168, Australia
    Diabetologia 52:1669-79. 2009

Collaborators

Detail Information

Publications23

  1. ncbi Role of macrophages in complications of type 2 diabetes
    G H Tesch
    Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Clin Exp Pharmacol Physiol 34:1016-9. 2007
    ..Novel strategies that are more specific at targeting macrophages may provide better protection against the development of Type 2 diabetic complications...
  2. ncbi Review: Serum and urine biomarkers of kidney disease: A pathophysiological perspective
    Greg H Tesch
    Department of Nephrology, Monash University, Monash Medical Centre, Clayton, Victoria, Australia
    Nephrology (Carlton) 15:609-16. 2010
    ..However, it does not explore the current status of these biomarkers in terms of their clinical validation...
  3. ncbi Macrophages and diabetic nephropathy
    Greg H Tesch
    Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Semin Nephrol 30:290-301. 2010
    ....
  4. ncbi MCP-1/CCL2: a new diagnostic marker and therapeutic target for progressive renal injury in diabetic nephropathy
    G H Tesch
    Dept of Nephrology, Monash Medical Centre, 246 Clayton Rd, Clayton, Victoria 3168, Australia
    Am J Physiol Renal Physiol 294:F697-701. 2008
    ..These findings provide a strong rationale for developing specific therapies against MCP-1 and inflammation in diabetic nephropathy...
  5. ncbi Rodent models of streptozotocin-induced diabetic nephropathy
    Greg H Tesch
    Department of Nephrology, Monash University, Monash Medical Centre, Clayton, Victoria, Australia
    Nephrology (Carlton) 12:261-6. 2007
    ....
  6. ncbi Role of MKK3-p38 MAPK signalling in the development of type 2 diabetes and renal injury in obese db/db mice
    A K H Lim
    Department of Nephrology, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia
    Diabetologia 52:347-58. 2009
    ..Therefore, this study examined whether MKK3 signalling influences the development of obesity, type 2 diabetes and diabetic nephropathy...
  7. ncbi Lymphocytes promote albuminuria, but not renal dysfunction or histological damage in a mouse model of diabetic renal injury
    A K H Lim
    Department of Nephrology, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia
    Diabetologia 53:1772-82. 2010
    ..While the importance of macrophages in diabetic renal injury has been clearly demonstrated, the role of lymphocytes is still unknown. We therefore examined the development of diabetic renal injury in lymphocyte-deficient mice...
  8. ncbi Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice
    F Y Chow
    Department of Nephrology, Monash Medical Centre, Clayton, Vic, 3168, Australia
    Diabetologia 50:471-80. 2007
    ..Based on these findings, the aim of this study was to examine whether a deficiency in MCP-1 would alter the development of type 2 diabetes and its renal complications...
  9. ncbi Monocyte chemoattractant protein-1 promotes the development of diabetic renal injury in streptozotocin-treated mice
    F Y Chow
    Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 69:73-80. 2006
    ..In conclusion, our study demonstrates that MCP-1-mediated macrophage accumulation and activation plays a critical role in the development of STZ-induced mouse diabetic nephropathy...
  10. ncbi Antibody blockade of c-fms suppresses the progression of inflammation and injury in early diabetic nephropathy in obese db/db mice
    A K H Lim
    Department of Nephrology, Monash Medical Centre, Clayton, Victoria 3168, Australia
    Diabetologia 52:1669-79. 2009
    ..Therefore, we used c-fms blockade as a strategy to selectively target macrophage-mediated injury during the progression of diabetic nephropathy...
  11. ncbi Recent insights into diabetic renal injury from the db/db mouse model of type 2 diabetic nephropathy
    G H Tesch
    Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia
    Am J Physiol Renal Physiol 300:F301-10. 2011
    ..This review summarizes the advances in knowledge gained from studies in genetically modified db/db mice and treatment of db/db mice with novel therapeutic agents...
  12. ncbi A pathogenic role for JNK signaling in experimental anti-GBM glomerulonephritis
    R S Flanc
    Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 72:698-708. 2007
    ..These studies suggest that JNK signaling promotes renal injury in acute and progressive rat anti-GBM disease. JNK inhibitors may be a novel therapeutic approach for the treatment of human glomerulonephritis...
  13. ncbi MKK3-p38 signaling promotes apoptosis and the early inflammatory response in the obstructed mouse kidney
    Frank Y Ma
    Department of Nephrology, Monash Medical Centre, 246 Clayton Rd, Clayton, Victoria 3168, Australia
    Am J Physiol Renal Physiol 293:F1556-63. 2007
    ..In conclusion, these studies identify discrete roles for MKK3-p38 signaling in renal cell apoptosis and the early inflammatory response in the obstructed kidney...
  14. ncbi LF15-0195 prevents the induction and inhibits the progression of rat anti-GBM disease
    G H Tesch
    Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia
    Kidney Int 60:1354-65. 2001
    ..This study examined whether LF15-0195 could suppress the induction and progression of rat anti-glomerular basement membrane (anti-GBM) glomerulonephritis...
  15. ncbi Interferon-gamma induces macrophage migration inhibitory factor synthesis and secretion by tubular epithelial cells
    Edwina K Rice
    Departments of Nephrology and Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    Nephrology (Carlton) 8:156-61. 2003
    ..These findings indicate that IFN-gamma induces rapid secretion of MIF by tubular epithelial cells, and suggest that this may be an important mechanism leading to inflammatory cell accumulation and activation during kidney disease...
  16. ncbi The role of p38alpha mitogen-activated protein kinase activation in renal fibrosis
    Cosimo Stambe
    Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia
    J Am Soc Nephrol 15:370-9. 2004
    ..Blockade of p38 MAPK reduces extracellular matrix production and may be considered a potential therapeutic option in the treatment of renal fibrosis...
  17. ncbi Blockade of p38alpha MAPK ameliorates acute inflammatory renal injury in rat anti-GBM glomerulonephritis
    Cosimo Stambe
    Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia
    J Am Soc Nephrol 14:338-51. 2003
    ..Blockade of the p38 pathway may be a novel therapeutic strategy for the treatment of acute renal inflammation...
  18. ncbi A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis
    Frank Y Ma
    Department of Nephrology, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia
    J Am Soc Nephrol 18:472-84. 2007
    ..Furthermore, JNK1 plays a nonredundant role in tubular cell apoptosis. These studies identify the JNK pathway as a potential therapeutic target in progressive kidney disease...
  19. ncbi Abnormal p38 mitogen-activated protein kinase signalling in human and experimental diabetic nephropathy
    L Adhikary
    Department of Nephrology, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia
    Diabetologia 47:1210-22. 2004
    ..Therefore, we examined whether p38 MAPK signalling is associated with the development of human and experimental diabetic nephropathy...
  20. ncbi Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat
    Frank Y Ma
    Department of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Victoria, Australia
    Lab Invest 89:470-84. 2009
    ..In conclusion, blockade of JNK signaling provides substantial protection against the progression of crescentic anti-GBM glomerulonephritis, which may be, in part, due to inhibition of the macrophage proinflammatory response...
  21. ncbi Lefty antagonises TGF-beta1 induced epithelial-mesenchymal transition in tubular epithelial cells
    Mythily Mariasegaram
    Department of Nephrology, Monash University, Monash Medical Centre, Clayton, Vic, Australia
    Biochem Biophys Res Commun 393:855-9. 2010
    ..In conclusion, Lefty can antagonise TGF-beta1 mediated EMT in renal tubular epithelial cells. Lefty may have potential as an anti-fibrotic molecule in the treatment of renal fibrosis...
  22. ncbi c-Jun amino terminal kinase 1 deficient mice are protected from streptozotocin-induced islet injury
    Kyoichi Fukuda
    Department of Nephrology, Monash Medical Centre, 246 Clayton Road, Clayton, 3168 Vic, Australia
    Biochem Biophys Res Commun 366:710-6. 2008
    ..In conclusion, JNK1 signaling plays an essential role in macrophage induced beta-cell apoptosis and the development of hyperglycemia in MLD-STZ induced pancreatic injury...
  23. ncbi MKK3 signalling plays an essential role in leukocyte-mediated pancreatic injury in the multiple low-dose streptozotocin model
    Kyoichi Fukuda
    Department of Nephrology, Monash Medical Centre, Clayton, Vic, Australia
    Lab Invest 88:398-407. 2008
    ..In conclusion, MKK3 signalling plays an essential role in the development of islet inflammation leading to destruction of beta-cells and hyperglycaemia in MLD-STZ-induced pancreatic injury...