Targeting the Endoplasmic Reticulum Unfolded Protein Response to Counteract the Oxidative Stress-Induced Endothelial Dysfunction
In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed...
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| Published in | Oxidative medicine and cellular longevity Vol. 2018; no. 2018; pp. 1 - 13 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Cairo, Egypt
Hindawi Publishing Corporation
01.01.2018
Hindawi John Wiley & Sons, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1942-0900 1942-0994 1942-0994 |
| DOI | 10.1155/2018/4946289 |
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| Abstract | In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the UPR pathways is the promotion of an adaptive response, the persistent activation of UPR leads to increased oxidative stress and cell death. This molecular switch has been correlated to the onset or to the exacerbation of the endothelial dysfunction in cardiovascular diseases. In this review, we highlight the multiple chances of the UPR to induce or ameliorate oxidative disturbances and propose the UPR pathways as a new therapeutic target for the clinical management of endothelial dysfunction. |
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| AbstractList | In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the UPR pathways is the promotion of an adaptive response, the persistent activation of UPR leads to increased oxidative stress and cell death. This molecular switch has been correlated to the onset or to the exacerbation of the endothelial dysfunction in cardiovascular diseases. In this review, we highlight the multiple chances of the UPR to induce or ameliorate oxidative disturbances and propose the UPR pathways as a new therapeutic target for the clinical management of endothelial dysfunction. In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the UPR pathways is the promotion of an adaptive response, the persistent activation of UPR leads to increased oxidative stress and cell death. This molecular switch has been correlated to the onset or to the exacerbation of the endothelial dysfunction in cardiovascular diseases. In this review, we highlight the multiple chances of the UPR to induce or ameliorate oxidative disturbances and propose the UPR pathways as a new therapeutic target for the clinical management of endothelial dysfunction.In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the UPR pathways is the promotion of an adaptive response, the persistent activation of UPR leads to increased oxidative stress and cell death. This molecular switch has been correlated to the onset or to the exacerbation of the endothelial dysfunction in cardiovascular diseases. In this review, we highlight the multiple chances of the UPR to induce or ameliorate oxidative disturbances and propose the UPR pathways as a new therapeutic target for the clinical management of endothelial dysfunction. |
| Audience | Academic |
| Author | Amodio, Giuseppina Faraonio, Raffaella Remondelli, Paolo Moltedo, Ornella |
| AuthorAffiliation | 1 Dipartimento di Medicina, Chirurgia e Odontoiatria “Scuola Medica Salernitana”, Università degli Studi di Salerno, 84081 Baronissi, Italy 2 Dipartimento di Farmacia, Università degli Studi di Salerno, 84084 Fisciano, Italy 3 Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli studi di Napoli “Federico II”, 80131 Naples, Italy |
| AuthorAffiliation_xml | – name: 3 Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli studi di Napoli “Federico II”, 80131 Naples, Italy – name: 1 Dipartimento di Medicina, Chirurgia e Odontoiatria “Scuola Medica Salernitana”, Università degli Studi di Salerno, 84081 Baronissi, Italy – name: 2 Dipartimento di Farmacia, Università degli Studi di Salerno, 84084 Fisciano, Italy |
| Author_xml | – sequence: 1 fullname: Remondelli, Paolo – sequence: 2 fullname: Faraonio, Raffaella – sequence: 3 fullname: Moltedo, Ornella – sequence: 4 fullname: Amodio, Giuseppina |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29725497$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | Copyright © 2018 Giuseppina Amodio et al. COPYRIGHT 2018 John Wiley & Sons, Inc. Copyright © 2018 Giuseppina Amodio et al.; This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2018 Giuseppina Amodio et al. 2018 |
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| Snippet | In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production... |
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| SubjectTerms | Antioxidants Apoptosis Cardiovascular diseases Cell death Chemical bonds Endoplasmic reticulum Endoplasmic Reticulum - metabolism Endothelial Cells - metabolism Endothelium Homeostasis Humans Kinases Medical research Medicine, Experimental Molecular biology Nitric oxide Oxidative stress Oxidative Stress - physiology Protein folding Quality control Review Rodents Transcription factors Unfolded Protein Response - physiology |
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| Title | Targeting the Endoplasmic Reticulum Unfolded Protein Response to Counteract the Oxidative Stress-Induced Endothelial Dysfunction |
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