Greg Tesch

Adj Assoc Prof

Accepting PhD Students

1992 …2019
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Personal profile


Research Interests. Diabetes and hypertension are major causes of end-stage kidney disease. Dr Tesch’s research focuses on identifying the underlying mechanisms of inflammation and fibrosis that are involved in kidney and heart injury in patients with diabetes and hypertension. In particular, his work focuses on the role of macrophages, tubular cells, fibroblasts and cell signalling pathways in progressive tissue injury. His studies utilize a variety of experimental techniques to examine the molecular mechanisms of disease, including conditional gene deletion, pharmacological blockade of receptors or intracellular signalling kinases, combination therapies, and cell culture studies. He is also engaged in a collaboration to develop novel drug delivery systems to target specific cell types. His previous work has led to clinical trials using an inhibitor of either a chemokine receptor (CCR2) or a specific kinase (ASK1) to treat diabetic kidney disease. This has been achieved through collaborations with local and overseas researchers, and with a number of commercial companies.

Research opportunities. We have a variety of projects available for PhD students and post-doctoral scientists examining novel mechanisms of inflammation and fibrosis in kidney disease. Our lab has an active PhD student program with 4 current students at different stages of their studies.

Research area keywords

  • Chronic Kidney Disease (CKD)
  • Diabetic Kidney Disease (DKD)
  • Glomerulonephritis
  • Cell signalling
  • Inflammation
  • Diabetic complications
  • Fibrosis

Network Recent external collaboration on country level. Dive into details by clicking on the dots.

Projects 2010 2019

Research Output 1992 2019

Combined inhibition of CCR2 and ACE provides added protection against progression of diabetic nephropathy in Nos3-deficient mice

Tesch, G. H., Pullen, N., Jesson, M. I., Schlerman, F. J. & Nikolic-Paterson, D. J., 1 Dec 2019, In : American Journal of Physiology - Renal Physiology. 317, 6, p. F1439-F1449 11 p.

Research output: Contribution to journalArticleResearchpeer-review

Establishing equivalent diabetes in male and female Nos3-deficient mice results in a comparable onset of diabetic kidney injury

Tian, L., Nikolic-Paterson, D. J. & Tesch, G. H., 1 Sep 2019, In : Physiological Reports. 7, 18, 8 p., e14197.

Research output: Contribution to journalArticleResearchpeer-review

Open Access
1 Citation (Scopus)

Pharmacological inhibition of protease-activated receptor-2 reduces crescent formation in rat nephrotoxic serum nephritis

Han, Y., Tian, L., Ma, F., Tesch, G., Vesey, D. A., Gobe, G. C., Lohman, R. J., Morais, C., Suen, J. Y., Fairlie, D. P. & Nikolic-Paterson, D. J., 1 May 2019, In : Clinical and Experimental Pharmacology and Physiology. 46, 5, p. 456-464 9 p.

Research output: Contribution to journalArticleResearchpeer-review

Proximal tubular epithelial cells preferentially endocytose covalently-modified albumin compared to native albumin

Ly, N. D. K., Tesch, G. H., Nikolic-Paterson, D. J. & Poronnik, P., Jan 2019, In : Nephrology. 24, 1, p. 121-126 6 p.

Research output: Contribution to journalArticleResearchpeer-review

6 Citations (Scopus)

ASK1 inhibitor treatment suppresses p38/JNK signalling with reduced kidney inflammation and fibrosis in rat crescentic glomerulonephritis

Amos, L. A., Ma, F. Y., Tesch, G. H., Liles, J. T., Breckenridge, D. G., Nikolic-Paterson, D. J. & Han, Y., 1 Sep 2018, In : Journal of Cellular and Molecular Medicine. 22, 9, p. 4522-4533 12 p.

Research output: Contribution to journalArticleResearchpeer-review

Open Access