The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Characterization of Susceptibility of Inbred Mouse Strains to Diabetic Nephropathy
Abstract
Differential susceptibility to diabetic nephropathy has been observed in humans, but it has not been well defined in inbred strains of mice. The present studies characterized the severity of diabetic nephropathy in six inbred mouse strains including C57BL/6J, DBA/2J, FVB/NJ, MRL/MpJ, A/J, and KK/HlJ mice. Diabetes mellitus was induced using low-dose streptozotocin injection. Progression of renal injury was evaluated by serial measurements of urinary albumin excretion, glomerular filtration rate (GFR), and terminal assessment of renal morphology over 25 weeks. Despite comparable levels of hyperglycemia, urinary albumin excretion and renal histopathological changes were dramatically different among strains. DBA/2J and KK/HlJ mice developed significantly more albuminuria than C57BL/6J, MRL/MpJ, and A/J mice. Severe glomerular mesangial expansion, nodular glomerulosclerosis, and arteriolar hyalinosis were observed in diabetic DBA/2J and KK/HlJ mice. Glomerular hyperfiltration was observed in all diabetic strains studied except A/J. The significant decline in GFR was not evident over the 25-week period of study, but diabetic DBA/2J mice exhibited a tendency for GFR to decline. Taken together, these results indicate that differential susceptibility to diabetic nephropathy exists in inbred mice. DBA/2J and KK/HlJ mice are more prone to diabetic nephropathy, whereas the most widely used C57BL/6J mice are relatively resistant to development of diabetic nephropathy.
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Cites
Finding genes that underlie complex traits.
Glazier, A. M., Nadeau, J. H., & Aitman, T. J. (2002) · Science · doi:10.1126/science.1076641 · Cited by 855
Targeted disruption of the chop gene delays endoplasmic reticulum stress-mediated diabetes
Oyadomari, S., Koizumi, A., Takeda, K., Gotoh, T., Akira, S., Araki, E., & Mori, M. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0214550 · Cited by 752
Proteotoxicity in the endoplasmic reticulum: Lessons from the Akita diabetic mouse
Ron, D. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0215020 · Cited by 133
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Non-Transgenic Mouse Models of Kidney Disease
Rabe, M., & Schaefer, F. (2016) · Nephron · doi:10.1159/000445171 · Cited by 1,922
Mouse Models of Diabetic Nephropathy
Brosius, F. C., Alpers, C. E., Bottinger, E. P., Breyer, M. D., Coffman, T. M., Gurley, S. B., Harris, R. C., Kakoki, M., Kretzler, M., Leiter, E. H., et al. (2009) · Journal of the American Society of Nephrology · doi:10.1681/asn.2009070721 · Cited by 895
Self-citationFujita, H., Morii, T., Fujishima, H., Sato, T., Shimizu, T., Hosoba, M., Tsukiyama, K., Narita, T., Takahashi, T., Drucker, D. J., et al. (2014) · Kidney International · doi:10.1038/ki.2013.427 · Cited by 336
Self-citationDisturbed glucose and pyruvate metabolism in glaucoma with neuroprotection by pyruvate or rapamycin
Harder, J. M., Guymer, C., Wood, J. P. M., Daskalaki, E., Chidlow, G., Zhang, C., Balasubramanian, R., Cardozo, B. H., Foxworth, N. E., Deering, K. E., et al. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2014213117 · Cited by 127
“D2 mice do not have hyperglycemia (21, 22), implying that retinal glucose metabolism itself is disrupted.”
Ghosh, S., Khazaei, M., Moien-Afshari, F., Ang, L. S., Granville, D. J., Verchere, C. B., Dunn, S. R., McCue, P., Mizisin, A., Sharma, K., et al. (2009) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.90548.2008 · Cited by 113
Metadata
- Authors
- Qi, Z., Fujita, H., Jin, J., Davis, L. S., Wang, Y., Fogo, A. B., & Breyer, M. D.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-09-01
- Volume
- 54
- Issue
- 9
- Pages
- 2628-2637
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2134975242
- Cited by
- 297
- References
- 3
- FWCI
- 7.63
- Type
- journal article
- Language
- en
- Open access
- closed
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