The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Inactivation of GSK-3β by Metallothionein Prevents Diabetes-Related Changes in Cardiac Energy Metabolism, Inflammation, Nitrosative Damage, and Remodeling
Open accessAbstract
OBJECTIVE: Glycogen synthase kinase (GSK)-3β plays an important role in cardiomyopathies. Cardiac-specific metallothionein-overexpressing transgenic (MT-TG) mice were highly resistant to diabetes-induced cardiomyopathy. Therefore, we investigated whether metallothionein cardiac protection against diabetes is mediated by inactivation of GSK-3β. RESEARCH DESIGN AND METHODS: Diabetes was induced with streptozotocin in both MT-TG and wild-type mice. Changes of energy metabolism–related molecules, lipid accumulation, inflammation, nitrosative damage, and fibrotic remodeling were examined in the hearts of diabetic mice 2 weeks, 2 months, and 5 months after the onset of diabetes with Western blotting, RT-PCR, and immunohistochemical assays. RESULTS: Activation (dephosphorylation) of GSK-3β was evidenced in the hearts of wild-type diabetic mice but not MT-TG diabetic mice. Correspondingly, cardiac glycogen synthase phosphorylation, hexokinase II, PPARα, and PGC-1α expression, which mediate glucose and lipid metabolisms, were significantly changed along with cardiac lipid accumulation, inflammation (TNF-α, plasminogen activator inhibitor 1 [PAI-1], and intracellular adhesion molecule 1 [ICAM-1]), nitrosative damage (3-nitrotyrosin accumulation), and fibrosis in the wild-type diabetic mice. The above pathological changes were completely prevented either by cardiac metallothionein in the MT-TG diabetic mice or by inhibition of GSK-3β activity in the wild-type diabetic mice with a GSK-3β–specific inhibitor. CONCLUSIONS: These results suggest that activation of GSK-3β plays a critical role in diabetes-related changes in cardiac energy metabolism, inflammation, nitrosative damage, and remodeling. Metallothionein inactivation of GSK-3β plays a critical role in preventing diabetic cardiomyopathy.
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Cites
Feige, J. N., Gelman, L., Michalik, L., Desvergne, B., & Wahli, W. (2006) · Progress in Lipid Research · doi:10.1016/j.plipres.2005.12.002 · Cited by 786 · cited 2×
“In general, however, PPAR expressions and activity are elevated in diabetes and reduced in both cardiac ischemia and hypertrophy (7,31,35).”
BackgroundNikoulina, S. E., Ciaraldi, T. P., Mudaliar, S., Mohideen, P., Carter, L., & Henry, R. R. (2000) · Diabetes · doi:10.2337/diabetes.49.2.263 · Cited by 357
Anderson, R. M., Barger, J. L., Edwards, M. G., Braun, K. H., O’Connor, C. E., Prolla, T. A., & Weindruch, R. (2008) · Aging Cell · doi:10.1111/j.1474-9726.2007.00357.x · Cited by 283 · cited 1×
“The finding of the inhibition of PGC-1 expression by inactivating GSK-3 is in line with results from other previous studies demonstrating that GSK-3 reduces PGC-1 expression by stimulating its proteasomal degradation (43).”
ResultCD36 Deficiency Rescues Lipotoxic Cardiomyopathy
Yang, J., Sambandam, N., Han, X., Gross, R. W., Courtois, M., Kovacs, A., Febbraio, M., Finck, B. N., & Kelly, D. P. (2007) · Circulation Research · doi:10.1161/01.res.0000264104.25265.b6 · Cited by 246
Transcriptional effects of chronic Akt activation in the heart
Cook, S. A., Matsui, T., Li, L., & Rosenzweig, A. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m201462200 · Cited by 199
Lehman, J. J., Boudina, S., Banke, N. H., Sambandam, N., Han, X., Young, D. M., Leone, T. C., Gross, R. W., Lewandowski, E. D., Abel, E. D., et al. (2008) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00081.2008 · Cited by 158
Whole body overexpression of PGC-1α has opposite effects on hepatic and muscle insulin sensitivity
Liang, H., Balas, B., Tantiwong, P., Dube, J., Goodpaster, B. H., O'Doherty, R. M., DeFronzo, R. A., Richardson, A., Musi, N., & Ward, W. F. (2009) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.90292.2008 · Cited by 81
Cited by
Chen, B., Yu, P., Chan, W. N., Xie, F., Zhang, Y., Liang, L., Leung, K. T., Lo, K. W., Yu, J., Tse, G. M. K., et al. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01679-y · Cited by 420
PPARα: Energy Combustion, Hypolipidemia, Inflammation and Cancer
Pyper, S. R., Viswakarma, N., Yu, S., & Reddy, J. K. (2010) · Nuclear Receptor Signaling · doi:10.1621/nrs.08002 · Cited by 379
Diabetes mellitus and Alzheimer's disease: GSK-3β as a potential link
Zhang, Y., Huang, N.-Q., Yan, F., Jin, H., Zhou, S.-Y., Shi, J.-S., & Jin, F. (2018) · Behavioural Brain Research · doi:10.1016/j.bbr.2017.11.015 · Cited by 301
The Role of Nrf2 in Cardiovascular Function and Disease
Satta, S., Mahmoud, A. M., Wilkinson, F. L., Yvonne Alexander, M., & White, S. J. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/9237263 · Cited by 293
Bai, Y., Cui, W., Xin, Y., Miao, X., Barati, M. T., Zhang, C., Chen, Q., Tan, Y., Cui, T., Zheng, Y., et al. (2013) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2013.01.008 · Cited by 274
Self-citation
Metadata
- Authors
- Wang, Y., Feng, W., Xue, W., Tan, Y., Hein, D. W., Li, X.-K., & Cai, L.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2009-03-26
- Volume
- 58
- Issue
- 6
- Pages
- 1391-1402
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2108359388
- Cited by
- 167
- References
- 7
- FWCI
- 5.34
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Wang, Y., Feng, W., Xue, W., Tan, Y., Hein, D. W., Li, X.-K., & Cai, L. (2009). Inactivation of GSK-3β by Metallothionein Prevents Diabetes-Related Changes in Cardiac Energy Metabolism, Inflammation, Nitrosative Damage, and Remodeling. Diabetes. https://doi.org/10.2337/db08-1697
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