The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Deletion of p66Shc Longevity Gene Protects Against Experimental Diabetic Glomerulopathy by Preventing Diabetes-Induced Oxidative Stress
Open accessAbstract
p66Shc regulates both steady-state and environmental stress-dependent reactive oxygen species (ROS) generation. Its deletion was shown to confer resistance to oxidative stress and protect mice from aging-associated vascular disease. This study was aimed at verifying the hypothesis that p66Shc deletion also protects from diabetic glomerulopathy by reducing oxidative stress. Streptozotocin-induced diabetic p66Shc knockout (KO) mice showed less marked changes in renal function and structure, as indicated by the significantly lower levels of proteinuria, albuminuria, glomerular sclerosis index, and glomerular and mesangial areas. Glomerular content of fibronectin and collagen IV was also lower in diabetic KO versus wild-type mice, whereas apoptosis was detected only in diabetic wild-type mice. Serum and renal tissue advanced glycation end products and plasma isoprostane 8-epi-prostaglandin F2α levels and activation of nuclear factor κB (NF-κB) were also lower in diabetic KO than in wild-type mice. Mesangial cells from KO mice grown under high-glucose conditions showed lower cell death rate, matrix production, ROS levels, and activation of NF-κB than those from wild-type mice. These data support a role for oxidative stress in the pathogenesis of diabetic glomerulopathy and indicate that p66Shc is involved in the molecular mechanism(s) underlying diabetes-induced oxidative stress and oxidant-dependent renal injury.
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Cites
Biochemistry and molecular cell biology of diabetic complications
Brownlee, M. (2001) · Nature · doi:10.1038/414813a · Cited by 9,107
Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage
Nishikawa, T., Edelstein, D., Du, X. L., Yamagishi, S.-I., Matsumura, T., Kaneda, Y., Yorek, M. A., Beebe, D., Oates, P. J., Hammes, H.-P., et al. (2000) · Nature · doi:10.1038/35008121 · Cited by 4,277
The p66shc adaptor protein controls oxidative stress response and life span in mammals
Migliaccio, E., Giorgio, M., Mele, S., Pelicci, G., Reboldi, P., Pandolfi, P. P., Lanfrancone, L., & Pelicci, P. G. (1999) · Nature · doi:10.1038/46311 · Cited by 1,712
Self-citationLander, H. M., Tauras, J. M., Ogiste, J. S., Hori, O., Moss, R. A., & Schmidt, A. M. (1997) · Journal of Biological Chemistry · doi:10.1074/jbc.272.28.17810 · Cited by 813
Hammes, H.-P., Du, X., Edelstein, D., Taguchi, T., Matsumura, T., Ju, Q., Lin, J., Bierhaus, A., Nawroth, P., Hannak, D., et al. (2003) · Nature Medicine · doi:10.1038/nm834 · Cited by 785
The Diabetes Control and Complications (DCCT) Research Group (1995) · Kidney International · doi:10.1038/ki.1995.236 · Cited by 694
Trinei, M., Giorgio, M., Cicalese, A., Barozzi, S., Ventura, A., Migliaccio, E., Milia, E., Padura, I. M., Raker, V. A., Maccarana, M., et al. (2002) · Oncogene · doi:10.1038/sj.onc.1205513 · Cited by 436
Self-citationInoguchi, T., Sonta, T., Tsubouchi, H., Etoh, T., Kakimoto, M., Sonoda, N., Sato, N., Sekiguchi, N., Kobayashi, K., Sumimoto, H., et al. (2003) · Journal of the American Society of Nephrology · doi:10.1097/01.asn.0000077407.90309.65 · Cited by 435
Napoli, C., Martin-Padura, I., de Nigris, F., Giorgio, M., Mansueto, G., Somma, P., Condorelli, M., Sica, G., De Rosa, G., & Pelicci, P. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0336359100 · Cited by 380
Self-citationDeletion of p66 shc Gene Protects Against Age-Related Endothelial Dysfunction
Francia, P., delli Gatti, C., Bachschmid, M., Martin-Padura, I., Savoia, C., Migliaccio, E., Pelicci, P. G., Schiavoni, M., Lüscher, T. F., Volpe, M., et al. (2004) · Circulation · doi:10.1161/01.cir.0000147731.24444.4d · Cited by 298 · cited 1×
“More recently, p66 ablation was found to protect from tissue damage (and apoptosis of endothelial cells and myofibers) following acute ischemia or ischemia/reperfusion (22) and endothelial dysfunction associated with aging (23).”
BackgroundSelf-citation
Cited by
Hydrogen peroxide: a metabolic by-product or a common mediator of ageing signals?
Giorgio, M., Trinei, M., Migliaccio, E., & Pelicci, P. G. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2240 · Cited by 1,447
Self-citationIncalza, M. A., D'Oria, R., Natalicchio, A., Perrini, S., Laviola, L., & Giorgino, F. (2018) · Vascular Pharmacology · doi:10.1016/j.vph.2017.05.005 · Cited by 1,356
Manolagas, S. C. (2010) · Endocrine Reviews · doi:10.1210/er.2009-0024 · Cited by 1,200
Kalogeris, T., Baines, C. P., Krenz, M., & Korthuis, R. J. (2016) · Comprehensive Physiology · doi:10.1002/cphy.c160006 · Cited by 718
Redox regulation of mitochondrial function
Handy, D. E., & Loscalzo, J. (2012) · Antioxidants & Redox Signaling · doi:10.1089/ars.2011.4123 · Cited by 588
Metadata
- Authors
- Menini, S., Amadio, L., Oddi, G., Ricci, C., Pesce, C., Pugliese, F., Giorgio, M., Migliaccio, E., Pelicci, P., Iacobini, C., & Pugliese, G.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2006-06-01
- Volume
- 55
- Issue
- 6
- Pages
- 1642-1650
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2112821970
- Cited by
- 183
- References
- 10
- FWCI
- 9.24
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Deletion of p66Shc Longevity Gene Protects Against Experimental Diabetic Glomerulopathy by Preventing Diabetes-Induced Oxidative Stress. https://app.cochat.ai/papers/10.2337/db05-1477
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- Menini, S., Amadio, L., Oddi, G., Ricci, C., Pesce, C., Pugliese, F., Giorgio, M., Migliaccio, E., Pelicci, P., Iacobini, C., & Pugliese, G. (2006). Deletion of p66Shc Longevity Gene Protects Against Experimental Diabetic Glomerulopathy by Preventing Diabetes-Induced Oxidative Stress. Diabetes. https://doi.org/10.2337/db05-1477
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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