G H Tesch

Summary

Affiliation: Monash University
Country: Australia

Publications

  1. ncbi request reprint 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
  2. doi request reprint 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
  3. doi request reprint 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. doi request reprint 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
  5. ncbi request reprint 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
  6. doi request reprint 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. doi request reprint 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 request reprint 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
  9. ncbi request reprint 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
  10. doi request reprint 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

Publications25

  1. ncbi request reprint 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
    ....
  2. doi request reprint 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...
  3. doi request reprint 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. doi request reprint 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...
  5. ncbi request reprint 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...
  6. doi request reprint 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. doi request reprint 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 request reprint 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...
  9. ncbi request reprint 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...
  10. doi request reprint 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 request reprint 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...
  12. doi request reprint 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...
  13. ncbi request reprint 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 request reprint 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 request reprint 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 request reprint 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 request reprint 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. doi request reprint CCL2-dependent macrophage recruitment is critical for mineralocorticoid receptor-mediated cardiac fibrosis, inflammation, and blood pressure responses in male mice
    J Z Shen
    Prince Henry s Institute of Medical Research J Z S, J M, P J F, M J Y Departments of Medicine J Z S, G H T, P J F, M J Y and Physiology M J Y, Monash University and Department of Nephrology G H T, Monash Medical Centre, Clayton 3168, Victoria, Australia
    Endocrinology 155:1057-66. 2014
    ..Our data thus demonstrate an important role for CCL2-dependent macrophage recruitment in MR-dependent cardiac inflammation and remodeling and in the regulation of systolic BP. ..
  19. ncbi request reprint 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...
  20. ncbi request reprint Aldosterone Induces Kidney Fibroblast Proliferation via Activation of Growth Factor Receptors and PI3K/MAPK Signalling
    L L Huang
    Department of Nephrology, Monash Medical Centre, Clayton, Vic, Australia
    Nephron Exp Nephrol 120:e115-e122. 2012
    ..This suggests that increased levels of aldosterone during disease may promote the severity of kidney fibrosis by inducing fibroblast proliferation...
  21. ncbi request reprint 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...
  22. doi request reprint 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...
  23. doi request reprint 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...
  24. ncbi request reprint 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...
  25. doi request reprint 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...