Pathogenesis of diabetic nephropathy
Open accessAbstract
As the increasing prevalence of diabetes reaches epidemic proportions worldwide, diabetic nephropathy and associated end-stage renal failure will be an unavoidable major health burden to not only individuals with diabetes and their families, but also to the health systems both in developed and developing countries. Over the past decade, a large body of research has focused on diabetic nephropathy ranging from studies in molecular signaling, hemodynamic regulation and pharmaceutical intervention to clinical outcomes. It is likely that the pathophysiology of diabetic nephropathy involves a multifactorial interaction between metabolic and hemodynamic factors. Metabolic factors involve glucose-dependent pathways, such as advanced glycation end-products and their receptors. Hemodynamic factors include various vasoactive hormones, such as components of the renin-angiotensin system. It is likely that these metabolic and hemodynamic factors interact through shared molecular and signaling pathways, such as nuclear factor kappa-light-chain-enhancer of activated B cells and protein kinase C with associated reactive oxygen species generation. It is likely that these contributing factors cause pathological damage not only to the glomerulus, in particular podocytes, but also to the tubulointerstitium. Specific inhibitors of the various pathways are now available and these emerging pharmaceutical interventions might have potential implications for the prevention and treatment of diabetic nephropathy. The mainstay of therapy remains the achievement of optimal glycemic and blood pressure control in order to slow the progression of diabetic nephropathy. Agents that interrupt the renin-angiotensin system have been shown to be particularly useful as renoprotective agents in both hypertensive and normotensive type 1 and type 2 diabetic subjects. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00131.x, 2011).
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The diabetic phenotype promotes diabetic nephropathy by inducing pathology in kidney cells directly involved with glomerular filtration; hyperglycemia promotes kidney fibrosis via activation of specific intracellular pathways.
“The diabetic phenotype also promotes DN by inducing pathology in kidney cells directly involved with glomerular filtration, as, for example, hyperglycemia promotes fibrosis in the kidney via inducing activation of specific intracellular pathways – the mechanisms by which T2D induces DN are reviewed in detail elsewhere.195,240”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [240]
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Oxidative Stress as a Major Culprit in Kidney Disease in Diabetes
Forbes, J. M., Coughlan, M. T., & Cooper, M. E. (2008) · Diabetes · doi:10.2337/db08-0057 · Cited by 1,203 · see citing works
Self-citationPathogenesis, prevention, and treatment of diabetic nephropathy
Cooper, M. E. (1998) · The Lancet · doi:10.1016/s0140-6736(98)01346-4 · Cited by 555 · see citing works
Self-citationMyocardial infarction increases ACE2 expression in rat and humans
Burrell, L. M., Risvanis, J., Kubota, E., Dean, R. G., Macdonald, P. S., Lu, L., Tikellis, C., Grant, S. L., Lew, R. A., Smith, A. I., et al. (2005) · European Heart Journal · doi:10.1093/eurheartj/ehi114 · Cited by 423 · see citing works
Self-citationInteraction of metabolic and haemodynamic factors in mediating experimental diabetic nephropathy
Cooper, M. E. (2001) · Diabetologia · doi:10.1007/s001250100000 · Cited by 375 · see citing works
Self-citationACE2, a new regulator of the renin–angiotensin system
Burrell, L. M., Johnston, C. I., Tikellis, C., & Cooper, M. E. (2004) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2004.03.001 · Cited by 362 · see citing works
Self-citationCharacterization of Renal Angiotensin-Converting Enzyme 2 in Diabetic Nephropathy
Tikellis, C., Johnston, C. I., Forbes, J. M., Burns, W. C., Burrell, L. M., Risvanis, J., & Cooper, M. E. (2003) · Hypertension · doi:10.1161/01.hyp.0000060689.38912.cb · Cited by 349 · see citing works
Self-citationThallas‐Bonke, V., Thorpe, S. R., Coughlan, M. T., Fukami, K., Yap, F. Y. T., Sourris, K. C., Penfold, S. A., Bach, L. A., Cooper, M. E., & Forbes, J. M. (2007) · Diabetes · doi:10.2337/db07-1119 · Cited by 345 · see citing works
Self-citationCooper, M. E., Boner, G., Cao, Z., et al. (2001) · Diabetologia · doi:10.1007/s001250100546 · Cited by 250 · see citing works
Self-citationThomas, M. C., Pickering, R. J., Tsorotes, D., Koı̈tka, A., Sheehy, K., Bernardi, S., Toffoli, B., Nguyen‐Huu, T., Head, G. A., Fu, Y., et al. (2010) · Circulation Research · doi:10.1161/circresaha.110.219279 · Cited by 230 · see citing works
Self-citationACE2 Deficiency Modifies Renoprotection Afforded by ACE Inhibition in Experimental Diabetes
Tikellis, C., Bialkowski, K., Pete, J., Sheehy, K., Qui, S., Johnston, C. I., Cooper, M. E., & Thomas, M. C. (2008) · Diabetes · doi:10.2337/db07-1212 · Cited by 182 · see citing works
Self-citationTikellis, C., Bernardi, S., & Burns, W. C. (2010) · Current Opinion in Nephrology & Hypertension · doi:10.1097/mnh.0b013e328341164a · Cited by 163 · see citing works
Cao, Z., Bonnet, F., Candido, R., et al. (2002) · Journal of the American Society of Nephrology · doi:10.1097/01.asn.0000019409.17099.33 · Cited by 120 · see citing works
Self-citationPrevention and treatment of diabetic nephropathy
Wittmann, I., Molnár, G. A., Degrell, P., Wagner, Z., Tamaskó, M., Laczy, B., Brasnyó, P., Wagner, L. J., & Nagy, J. (2005) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2005.03.011 · Cited by 116 · see citing works
Radke, J. R., Donald, R. G. K., Eibs, A., et al. (2006) · PLoS Pathogens · doi:10.1371/journal.ppat.0020105 · Cited by 101 · see citing works
Forbes, J. M., Bonnet, F., Russo, L. M., Burns, W. C., Cao, Z., Candido, R., Kawachi, H., Allen, T. J., Cooper, M. E., Jerums, G., et al. (2002) · Journal of Hypertension · doi:10.1097/00004872-200205000-00034 · Cited by 89 · see citing works
Self-citationSET-related Cell Division Autoantigen-1 (CDA1) Arrests Cell Growth
Chai, Z., Šarčević, B., Mawson, A., et al. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m007681200 · Cited by 85 · see citing works
Tu, Y., Wu, W., Wu, T., Cao, Z., Wilkins, R. J., Toh, B. H., Cooper, M. E., & Chai, Z. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m609623200 · Cited by 70 · see citing works
Self-citationIto, T., Tsukumo, S., Suzuki, N., Motohashi, H., Yamamoto, M. P., Fujii‐Kuriyama, Y., Mimura, J., Lin, T.-M., Peterson, R. E., Tohyama, C., et al. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m402143200 · Cited by 69 · see citing works
Davis, B. J., Cao, Z., Marc De Gasparo, B., Kawachi, H., Cooper, M. E., & Allen, T. J. (2003) · Journal of Hypertension · doi:10.1097/00004872-200301000-00031 · Cited by 69 · see citing works
Self-citationANGIOTENSIN CONVERTING ENZYME 2 IN THE KIDNEY
Koı̈tka, A., Cooper, M. E., Thomas, M. C., & Tikellis, C. (2008) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/j.1440-1681.2008.04889.x · Cited by 48 · see citing works
Self-citationPolymorphisms in the gene encoding angiotensin I converting enzyme 2 and diabetic nephropathy
Fröjdö, S., Sjölind, L., Parkkonen, M., et al. (2005) · Diabetologia · doi:10.1007/s00125-005-1955-4 · Cited by 37 · see citing works
Pham, Y., Tu, Y., Wu, T., et al. (2009) · Diabetologia · doi:10.1007/s00125-009-1555-9 · Cited by 35 · see citing works
Tu, Y., Wu, T., Dai, A., et al. (2010) · Kidney International · doi:10.1038/ki.2010.374 · Cited by 30 · see citing works
Role of Cell Division Autoantigen 1 (CDA1) in Cell Proliferation and Fibrosis
Toh, B., Tu, Y., Cao, Z., Cooper, M. E., & Chai, Z. (2010) · Genes · doi:10.3390/genes1030335 · Cited by 15 · see citing works
Self-citationNEPHRIN EXPRESSION IN THE POST-NATAL DEVELOPING KIDNEY IN NORMOTENSIVE AND HYPERTENSIVE RATS
Bonnet, F., Tikellis, C., Kawachi, H., et al. (2002) · Clinical and Experimental Hypertension · doi:10.1081/ceh-120004798 · Cited by 15 · see citing works
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Sturmlechner, I., Durik, M., Sieben, C. J., Baker, D. J., & van Deursen, J. M. (2017) · Nature Reviews Nephrology · doi:10.1038/nrneph.2016.183 · Cited by 345 · see citing works
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Yang, D., Livingston, M. J., Liu, Z., Dong, G., Zhang, M., Chen, J.-K., & Dong, Z. (2018) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2639-1 · Cited by 252 · see citing works
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Wang, J., Xiang, H., Lu, Y., Wu, T., & Ji, G. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.111918 · Cited by 74 · see citing works
Nascimento, M., Punaro, G. R., Serralha, R. S., Lima, D. Y., Mouro, M. G., Oliveira, L. C. G., Casarini, D. E., Rodrigues, A. M., & Higa, E. M. S. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.117640 · Cited by 12 · see citing works
- Authors
- Cao, Z., & Cooper, M. E.
- Affiliations
- Baker Heart and Diabetes Institute (AU)
- Corresponding author
- Cooper, Mark E
- ORCID
- Cooper, Mark E
- Venue
- Journal of Diabetes Investigation
- Publisher
- Wiley
- Published
- 2011-06-06
- Volume
- 2
- Issue
- 4
- Pages
- 243-247
- ISSN
- 2040-1116 (ISSN-L)
- PMC
- PMC4014960
- OpenAlex
- W1586904317
- Cited by
- 219
- References
- 25
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 16 · 2023: 20 · 2022: 28 · 2021: 34 · 2020: 27 · 2019: 18 · 2018: 14 · 2017: 14 · 2016: 7 · 2015: 5 · 2014: 5 · 2013: 7 · 2012: 4
- FWCI
- 4.22
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Diabetes Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart Foundation of Australia
- Ministerio de Economía y Competitividad
- Medical Research Council
- National Health and Medical Research Council
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Keywords
- diabetic nephropathy, pathogenesis, advanced glycation end products, renin-angiotensin system, NF-κB, protein kinase C, reactive oxygen species, podocytes, glomerular injury, tubulointerstitial injury, glycemic control, blood pressure control, type 1 diabetes, type 2 diabetes, end-stage renal disease
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