The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis
Cellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the...
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-12-01
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| Series: | Life |
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| Online Access: | https://www.mdpi.com/2075-1729/11/1/1 |
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| author | Mahmoud Aghaei Sanaz Dastghaib Sajjad Aftabi Mohamad-Reza Aghanoori Javad Alizadeh Pooneh Mokarram Parvaneh Mehrbod Milad Ashrafizadeh Ali Zarrabi Kielan Darcy McAlinden Mathew Suji Eapen Sukhwinder Singh Sohal Pawan Sharma Amir A. Zeki Saeid Ghavami |
| author_facet | Mahmoud Aghaei Sanaz Dastghaib Sajjad Aftabi Mohamad-Reza Aghanoori Javad Alizadeh Pooneh Mokarram Parvaneh Mehrbod Milad Ashrafizadeh Ali Zarrabi Kielan Darcy McAlinden Mathew Suji Eapen Sukhwinder Singh Sohal Pawan Sharma Amir A. Zeki Saeid Ghavami |
| author_sort | Mahmoud Aghaei |
| collection | DOAJ |
| description | Cellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the increased functional demands. Cells are able to induce a highly conserved adaptive mechanism, known as the unfolded protein response (UPR), to manage such stresses. UPR dysregulation and ER stress are involved in numerous human illnesses, such as metabolic syndrome, fibrotic diseases, and neurodegeneration, and cancer. Therefore, effective and specific compounds targeting the UPR pathway are being considered as potential therapies. This review focuses on the impact of both external and internal stressors on the ER in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) and discusses the role of the UPR signaling pathway activation in the control of cellular damage and specifically highlights the potential involvement of non-coding RNAs in COPD. Summaries of pathogenic mechanisms associated with the ER stress/UPR axis contributing to IPF and COPD, and promising pharmacological intervention strategies, are also presented. |
| first_indexed | 2024-04-11T09:45:55Z |
| format | Article |
| id | doaj.art-fa66fb79d825476b823e4d522cb28f1b |
| institution | Directory Open Access Journal |
| issn | 2075-1729 |
| language | English |
| last_indexed | 2024-04-11T09:45:55Z |
| publishDate | 2020-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Life |
| spelling | doaj.art-fa66fb79d825476b823e4d522cb28f1b2022-12-22T04:31:01ZengMDPI AGLife2075-17292020-12-01111110.3390/life11010001The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary FibrosisMahmoud Aghaei0Sanaz Dastghaib1Sajjad Aftabi2Mohamad-Reza Aghanoori3Javad Alizadeh4Pooneh Mokarram5Parvaneh Mehrbod6Milad Ashrafizadeh7Ali Zarrabi8Kielan Darcy McAlinden9Mathew Suji Eapen10Sukhwinder Singh Sohal11Pawan Sharma12Amir A. Zeki13Saeid Ghavami14Department of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R3E 0J9, CanadaDepartment of Clinical Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz 7134845794, IranDepartment of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R3E 0J9, CanadaDivision of Neurodegenerative Disorders, St Boniface Hospital Albrechtsen Research Centre, University of Manitoba, Winnipeg, MB R2H 2A6, CanadaDepartment of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R3E 0J9, CanadaDepartment of Clinical Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz 7134845794, IranInfluenza and Respiratory Viruses Department, Pasteur Institute of Iran, Tehran 1316943551, IranFaculty of Engineering and Natural Sciences, Sabanci University, Orta Mahalle, Üniversite Caddesi No. 27, Orhanlı, Tuzla, 34956 Istanbul, TurkeySabanci University Nanotechnology Research and Application Center (SUNUM), Tuzla, 34956 Istanbul, TurkeyRespiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, University of Tasmania, Launceston 7250, Tasmania, AustraliaRespiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, University of Tasmania, Launceston 7250, Tasmania, AustraliaRespiratory Translational Research Group, Department of Laboratory Medicine, School of Health Sciences, University of Tasmania, Launceston 7250, Tasmania, AustraliaCenter for Translational Medicine, Jane & Leonard Korman Respiratory Institute, Thomas Jefferson University, Philadelphia, PA 19107, USADavis School of Medicine, Department of Internal Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, UC Davis Lung Center, University of California, Davis, CA 95616, USADepartment of Human Anatomy and Cell Science, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R3E 0J9, CanadaCellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the increased functional demands. Cells are able to induce a highly conserved adaptive mechanism, known as the unfolded protein response (UPR), to manage such stresses. UPR dysregulation and ER stress are involved in numerous human illnesses, such as metabolic syndrome, fibrotic diseases, and neurodegeneration, and cancer. Therefore, effective and specific compounds targeting the UPR pathway are being considered as potential therapies. This review focuses on the impact of both external and internal stressors on the ER in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) and discusses the role of the UPR signaling pathway activation in the control of cellular damage and specifically highlights the potential involvement of non-coding RNAs in COPD. Summaries of pathogenic mechanisms associated with the ER stress/UPR axis contributing to IPF and COPD, and promising pharmacological intervention strategies, are also presented.https://www.mdpi.com/2075-1729/11/1/1endoplasmic reticulumfibrosistissue remodelingnon-coding RNAUPRautophagy |
| spellingShingle | Mahmoud Aghaei Sanaz Dastghaib Sajjad Aftabi Mohamad-Reza Aghanoori Javad Alizadeh Pooneh Mokarram Parvaneh Mehrbod Milad Ashrafizadeh Ali Zarrabi Kielan Darcy McAlinden Mathew Suji Eapen Sukhwinder Singh Sohal Pawan Sharma Amir A. Zeki Saeid Ghavami The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis Life endoplasmic reticulum fibrosis tissue remodeling non-coding RNA UPR autophagy |
| title | The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis |
| title_full | The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis |
| title_fullStr | The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis |
| title_full_unstemmed | The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis |
| title_short | The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis |
| title_sort | er stress upr axis in chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis |
| topic | endoplasmic reticulum fibrosis tissue remodeling non-coding RNA UPR autophagy |
| url | https://www.mdpi.com/2075-1729/11/1/1 |
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