Oxidative Stress, Apoptosis, and Mitochondrial Function in Diabetic Nephropathy
Diabetic nephropathy (DN) is the second most frequent and prevalent complication of diabetes mellitus (DM). The increase in the production of oxidative stress (OS) is induced by the persistent hyperglycemic state capable of producing oxidative damage to the macromolecules (lipids, carbohydrates, pro...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | International Journal of Endocrinology |
| Online Access: | http://dx.doi.org/10.1155/2018/1875870 |
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| author | Sonia Sifuentes-Franco Diego Enrique Padilla-Tejeda Sandra Carrillo-Ibarra Alejandra Guillermina Miranda-Díaz |
| author_facet | Sonia Sifuentes-Franco Diego Enrique Padilla-Tejeda Sandra Carrillo-Ibarra Alejandra Guillermina Miranda-Díaz |
| author_sort | Sonia Sifuentes-Franco |
| collection | DOAJ |
| description | Diabetic nephropathy (DN) is the second most frequent and prevalent complication of diabetes mellitus (DM). The increase in the production of oxidative stress (OS) is induced by the persistent hyperglycemic state capable of producing oxidative damage to the macromolecules (lipids, carbohydrates, proteins, and nucleic acids). OS favors the production of oxidative damage to the histones of the double-chain DNA and affects expression of the DNA repairer enzyme which leads to cell death from apoptosis. The chronic hyperglycemic state unchains an increase in advanced glycation end-products (AGE) that interact through the cellular receptors to favor activation of the transcription factor NF-κB and the protein kinase C (PKC) system, leading to the appearance of inflammation, growth, and augmentation of synthesis of the extracellular matrix (ECM) in DN. The reactive oxygen species (ROS) play an important role in the pathogenesis of diabetic complications because the production of ROS increases during the persistent hyperglycemia. The primary source of the excessive production of ROS is the mitochondria with the capacity to exceed production of endogenous antioxidants. Due to the fact that the mechanisms involved in the development of DN have not been fully clarified, there are different approaches to specific therapeutic targets or adjuvant management alternatives in the control of glycemia in DN. |
| format | Article |
| id | doaj-art-0423d3a598bc414fa8a7315fb65e5f7c |
| institution | OA Journals |
| issn | 1687-8337 1687-8345 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Endocrinology |
| spelling | doaj-art-0423d3a598bc414fa8a7315fb65e5f7c2025-08-20T02:03:06ZengWileyInternational Journal of Endocrinology1687-83371687-83452018-01-01201810.1155/2018/18758701875870Oxidative Stress, Apoptosis, and Mitochondrial Function in Diabetic NephropathySonia Sifuentes-Franco0Diego Enrique Padilla-Tejeda1Sandra Carrillo-Ibarra2Alejandra Guillermina Miranda-Díaz3Institute of Experimental and Clinical Therapeutics, Department of Physiology, University Health Sciences Centre, University of Guadalajara, Guadalajara, JAL, MexicoPrograma de Químico Farmacéutico Biotecnologo, Escuela de Ciencias de la Salud, Campus Zapopan, Universidad del Valle de México, Guadalajara, JAL, MexicoInstitute of Experimental and Clinical Therapeutics, Department of Physiology, University Health Sciences Centre, University of Guadalajara, Guadalajara, JAL, MexicoInstitute of Experimental and Clinical Therapeutics, Department of Physiology, University Health Sciences Centre, University of Guadalajara, Guadalajara, JAL, MexicoDiabetic nephropathy (DN) is the second most frequent and prevalent complication of diabetes mellitus (DM). The increase in the production of oxidative stress (OS) is induced by the persistent hyperglycemic state capable of producing oxidative damage to the macromolecules (lipids, carbohydrates, proteins, and nucleic acids). OS favors the production of oxidative damage to the histones of the double-chain DNA and affects expression of the DNA repairer enzyme which leads to cell death from apoptosis. The chronic hyperglycemic state unchains an increase in advanced glycation end-products (AGE) that interact through the cellular receptors to favor activation of the transcription factor NF-κB and the protein kinase C (PKC) system, leading to the appearance of inflammation, growth, and augmentation of synthesis of the extracellular matrix (ECM) in DN. The reactive oxygen species (ROS) play an important role in the pathogenesis of diabetic complications because the production of ROS increases during the persistent hyperglycemia. The primary source of the excessive production of ROS is the mitochondria with the capacity to exceed production of endogenous antioxidants. Due to the fact that the mechanisms involved in the development of DN have not been fully clarified, there are different approaches to specific therapeutic targets or adjuvant management alternatives in the control of glycemia in DN.http://dx.doi.org/10.1155/2018/1875870 |
| spellingShingle | Sonia Sifuentes-Franco Diego Enrique Padilla-Tejeda Sandra Carrillo-Ibarra Alejandra Guillermina Miranda-Díaz Oxidative Stress, Apoptosis, and Mitochondrial Function in Diabetic Nephropathy International Journal of Endocrinology |
| title | Oxidative Stress, Apoptosis, and Mitochondrial Function in Diabetic Nephropathy |
| title_full | Oxidative Stress, Apoptosis, and Mitochondrial Function in Diabetic Nephropathy |
| title_fullStr | Oxidative Stress, Apoptosis, and Mitochondrial Function in Diabetic Nephropathy |
| title_full_unstemmed | Oxidative Stress, Apoptosis, and Mitochondrial Function in Diabetic Nephropathy |
| title_short | Oxidative Stress, Apoptosis, and Mitochondrial Function in Diabetic Nephropathy |
| title_sort | oxidative stress apoptosis and mitochondrial function in diabetic nephropathy |
| url | http://dx.doi.org/10.1155/2018/1875870 |
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