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Protective role of NRF2 in macrovascular complications of diabetes
Macrovascular complications develop in over a half of the diabetic individuals, resulting in high morbidity and mortality. This poses a severe threat to public health and a heavy burden to social economy. It is therefore important to develop effective approaches to prevent or slow down the pathogene...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7417734/ https://www.ncbi.nlm.nih.gov/pubmed/32628815 http://dx.doi.org/10.1111/jcmm.15583 |
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author | Wu, Junduo Sun, Xiaodan Jiang, Ziping Jiang, Jun Xu, Linlin Tian, Ao Sun, Xuechun Meng, Huali Li, Ying Huang, Wenlin Jia, Ye Wu, Hao |
author_facet | Wu, Junduo Sun, Xiaodan Jiang, Ziping Jiang, Jun Xu, Linlin Tian, Ao Sun, Xuechun Meng, Huali Li, Ying Huang, Wenlin Jia, Ye Wu, Hao |
author_sort | Wu, Junduo |
collection | PubMed |
description | Macrovascular complications develop in over a half of the diabetic individuals, resulting in high morbidity and mortality. This poses a severe threat to public health and a heavy burden to social economy. It is therefore important to develop effective approaches to prevent or slow down the pathogenesis and progression of macrovascular complications of diabetes (MCD). Oxidative stress is a major contributor to MCD. Nuclear factor (erythroid‐derived 2)‐like 2 (NRF2) governs cellular antioxidant defence system by activating the transcription of various antioxidant genes, combating diabetes‐induced oxidative stress. Accumulating experimental evidence has demonstrated that NRF2 activation protects against MCD. Structural inhibition of Kelch‐like ECH‐associated protein 1 (KEAP1) is a canonical way to activate NRF2. More recently, novel approaches, such as activation of the Nfe2l2 gene transcription, decreasing KEAP1 protein level by microRNA‐induced degradation of Keap1 mRNA, prevention of proteasomal degradation of NRF2 protein and modulation of other upstream regulators of NRF2, have emerged in prevention of MCD. This review provides a brief introduction of the pathophysiology of MCD and the role of oxidative stress in the pathogenesis of MCD. By reviewing previous work on the activation of NRF2 in MCD, we summarize strategies to activate NRF2, providing clues for future intervention of MCD. Controversies over NRF2 activation and future perspectives are also provided in this review. |
format | Online Article Text |
id | pubmed-7417734 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-74177342020-08-11 Protective role of NRF2 in macrovascular complications of diabetes Wu, Junduo Sun, Xiaodan Jiang, Ziping Jiang, Jun Xu, Linlin Tian, Ao Sun, Xuechun Meng, Huali Li, Ying Huang, Wenlin Jia, Ye Wu, Hao J Cell Mol Med Reviews Macrovascular complications develop in over a half of the diabetic individuals, resulting in high morbidity and mortality. This poses a severe threat to public health and a heavy burden to social economy. It is therefore important to develop effective approaches to prevent or slow down the pathogenesis and progression of macrovascular complications of diabetes (MCD). Oxidative stress is a major contributor to MCD. Nuclear factor (erythroid‐derived 2)‐like 2 (NRF2) governs cellular antioxidant defence system by activating the transcription of various antioxidant genes, combating diabetes‐induced oxidative stress. Accumulating experimental evidence has demonstrated that NRF2 activation protects against MCD. Structural inhibition of Kelch‐like ECH‐associated protein 1 (KEAP1) is a canonical way to activate NRF2. More recently, novel approaches, such as activation of the Nfe2l2 gene transcription, decreasing KEAP1 protein level by microRNA‐induced degradation of Keap1 mRNA, prevention of proteasomal degradation of NRF2 protein and modulation of other upstream regulators of NRF2, have emerged in prevention of MCD. This review provides a brief introduction of the pathophysiology of MCD and the role of oxidative stress in the pathogenesis of MCD. By reviewing previous work on the activation of NRF2 in MCD, we summarize strategies to activate NRF2, providing clues for future intervention of MCD. Controversies over NRF2 activation and future perspectives are also provided in this review. John Wiley and Sons Inc. 2020-07-06 2020-08 /pmc/articles/PMC7417734/ /pubmed/32628815 http://dx.doi.org/10.1111/jcmm.15583 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Reviews Wu, Junduo Sun, Xiaodan Jiang, Ziping Jiang, Jun Xu, Linlin Tian, Ao Sun, Xuechun Meng, Huali Li, Ying Huang, Wenlin Jia, Ye Wu, Hao Protective role of NRF2 in macrovascular complications of diabetes |
title | Protective role of NRF2 in macrovascular complications of diabetes |
title_full | Protective role of NRF2 in macrovascular complications of diabetes |
title_fullStr | Protective role of NRF2 in macrovascular complications of diabetes |
title_full_unstemmed | Protective role of NRF2 in macrovascular complications of diabetes |
title_short | Protective role of NRF2 in macrovascular complications of diabetes |
title_sort | protective role of nrf2 in macrovascular complications of diabetes |
topic | Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7417734/ https://www.ncbi.nlm.nih.gov/pubmed/32628815 http://dx.doi.org/10.1111/jcmm.15583 |
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