Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis
Idiopathic pulmonary fibrosis (IPF), the most common form of idiopathic interstitial pneumonia, is a progressive, irreversible, and typically lethal disease characterized by an abnormal fibrotic response involving vast areas of the lungs. Given the poor knowledge of the mechanisms underpinning IPF o...
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| Published in | Cellular and molecular life sciences : CMLS Vol. 78; no. 5; pp. 2031 - 2057 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Cham
Springer International Publishing
01.03.2021
Springer Nature B.V |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1420-682X 1420-9071 1420-9071 |
| DOI | 10.1007/s00018-020-03693-7 |
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| Abstract | Idiopathic pulmonary fibrosis (IPF), the most common form of idiopathic interstitial pneumonia, is a progressive, irreversible, and typically lethal disease characterized by an abnormal fibrotic response involving vast areas of the lungs. Given the poor knowledge of the mechanisms underpinning IPF onset and progression, a better understanding of the cellular processes and molecular pathways involved is essential for the development of effective therapies, currently lacking. Besides a number of established IPF-associated risk factors, such as cigarette smoking, environmental factors, comorbidities, and viral infections, several other processes have been linked with this devastating disease. Apoptosis, senescence, epithelial-mesenchymal transition, endothelial-mesenchymal transition, and epithelial cell migration have been shown to play a key role in IPF-associated tissue remodeling. Moreover, molecules, such as chemokines, cytokines, growth factors, adenosine, glycosaminoglycans, non-coding RNAs, and cellular processes including oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, hypoxia, and alternative polyadenylation have been linked with IPF development. Importantly, strategies targeting these processes have been investigated to modulate abnormal cellular phenotypes and maintain tissue homeostasis in the lung. This review provides an update regarding the emerging cellular and molecular mechanisms involved in the onset and progression of IPF. |
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| AbstractList | Idiopathic pulmonary fibrosis (IPF), the most common form of idiopathic interstitial pneumonia, is a progressive, irreversible, and typically lethal disease characterized by an abnormal fibrotic response involving vast areas of the lungs. Given the poor knowledge of the mechanisms underpinning IPF onset and progression, a better understanding of the cellular processes and molecular pathways involved is essential for the development of effective therapies, currently lacking. Besides a number of established IPF-associated risk factors, such as cigarette smoking, environmental factors, comorbidities, and viral infections, several other processes have been linked with this devastating disease. Apoptosis, senescence, epithelial-mesenchymal transition, endothelial-mesenchymal transition, and epithelial cell migration have been shown to play a key role in IPF-associated tissue remodeling. Moreover, molecules, such as chemokines, cytokines, growth factors, adenosine, glycosaminoglycans, non-coding RNAs, and cellular processes including oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, hypoxia, and alternative polyadenylation have been linked with IPF development. Importantly, strategies targeting these processes have been investigated to modulate abnormal cellular phenotypes and maintain tissue homeostasis in the lung. This review provides an update regarding the emerging cellular and molecular mechanisms involved in the onset and progression of IPF. Idiopathic pulmonary fibrosis (IPF), the most common form of idiopathic interstitial pneumonia, is a progressive, irreversible, and typically lethal disease characterized by an abnormal fibrotic response involving vast areas of the lungs. Given the poor knowledge of the mechanisms underpinning IPF onset and progression, a better understanding of the cellular processes and molecular pathways involved is essential for the development of effective therapies, currently lacking. Besides a number of established IPF-associated risk factors, such as cigarette smoking, environmental factors, comorbidities, and viral infections, several other processes have been linked with this devastating disease. Apoptosis, senescence, epithelial-mesenchymal transition, endothelial-mesenchymal transition, and epithelial cell migration have been shown to play a key role in IPF-associated tissue remodeling. Moreover, molecules, such as chemokines, cytokines, growth factors, adenosine, glycosaminoglycans, non-coding RNAs, and cellular processes including oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, hypoxia, and alternative polyadenylation have been linked with IPF development. Importantly, strategies targeting these processes have been investigated to modulate abnormal cellular phenotypes and maintain tissue homeostasis in the lung. This review provides an update regarding the emerging cellular and molecular mechanisms involved in the onset and progression of IPF.Idiopathic pulmonary fibrosis (IPF), the most common form of idiopathic interstitial pneumonia, is a progressive, irreversible, and typically lethal disease characterized by an abnormal fibrotic response involving vast areas of the lungs. Given the poor knowledge of the mechanisms underpinning IPF onset and progression, a better understanding of the cellular processes and molecular pathways involved is essential for the development of effective therapies, currently lacking. Besides a number of established IPF-associated risk factors, such as cigarette smoking, environmental factors, comorbidities, and viral infections, several other processes have been linked with this devastating disease. Apoptosis, senescence, epithelial-mesenchymal transition, endothelial-mesenchymal transition, and epithelial cell migration have been shown to play a key role in IPF-associated tissue remodeling. Moreover, molecules, such as chemokines, cytokines, growth factors, adenosine, glycosaminoglycans, non-coding RNAs, and cellular processes including oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, hypoxia, and alternative polyadenylation have been linked with IPF development. Importantly, strategies targeting these processes have been investigated to modulate abnormal cellular phenotypes and maintain tissue homeostasis in the lung. This review provides an update regarding the emerging cellular and molecular mechanisms involved in the onset and progression of IPF. |
| Author | Pintus, Gianfranco Paliogiannis, Panagiotis Zinellu, Angelo Eid, Ali Hussein Mangoni, Arduino Aleksander Nasrallah, Gheyath K. Giordo, Roberta Phan, Thị Hằng Giang Fois, Alessandro Giuseppe |
| Author_xml | – sequence: 1 givenname: Thị Hằng Giang surname: Phan fullname: Phan, Thị Hằng Giang organization: Department of Immunology and Pathophysiology, University of Medicine and Pharmacy, Hue University – sequence: 2 givenname: Panagiotis surname: Paliogiannis fullname: Paliogiannis, Panagiotis organization: Department of Medical, Surgical and Experimental Sciences, University of Sassari – sequence: 3 givenname: Gheyath K. surname: Nasrallah fullname: Nasrallah, Gheyath K. email: gheyath.nasrallah@qu.edu.qa organization: Department of Biomedical Sciences, College of Health Sciences Member of QU Health, Qatar University, Biomedical Research Center Qatar University – sequence: 4 givenname: Roberta surname: Giordo fullname: Giordo, Roberta organization: Department of Medical Laboratory Sciences, College of Health Sciences, and Sharjah Institute for Medical Research, University of Sharjah – sequence: 5 givenname: Ali Hussein surname: Eid fullname: Eid, Ali Hussein organization: Department of Basic Medical Sciences, College of Medicine, QU Health, Qatar University, Biomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut – sequence: 6 givenname: Alessandro Giuseppe surname: Fois fullname: Fois, Alessandro Giuseppe organization: Department of Medical, Surgical and Experimental Sciences, University of Sassari – sequence: 7 givenname: Angelo surname: Zinellu fullname: Zinellu, Angelo organization: Department of Biomedical Sciences, University of Sassari – sequence: 8 givenname: Arduino Aleksander surname: Mangoni fullname: Mangoni, Arduino Aleksander email: arduino.mangoni@flinders.edu.au organization: Department of Clinical Pharmacology, College of Medicine and Public Health, Flinders University – sequence: 9 givenname: Gianfranco orcidid: 0000-0002-3031-7733 surname: Pintus fullname: Pintus, Gianfranco email: gpintus@sharjah.ac.ae organization: Department of Medical Laboratory Sciences, College of Health Sciences, and Sharjah Institute for Medical Research, University of Sharjah, Department of Biomedical Sciences, University of Sassari |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33201251$$D View this record in MEDLINE/PubMed |
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| Snippet | Idiopathic pulmonary fibrosis (IPF), the most common form of idiopathic interstitial pneumonia, is a progressive, irreversible, and typically lethal disease... |
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| SubjectTerms | Adenosine Apoptosis Apoptosis - genetics Apoptosis - physiology Biochemistry Biomedical and Life Sciences Biomedicine Cell adhesion & migration Cell Biology Cell migration cell movement Chemokines Cigarette smoking cigarettes Cytokines Endoplasmic reticulum endoplasmic reticulum stress Endoplasmic Reticulum Stress - genetics Endoplasmic Reticulum Stress - physiology Environmental factors Epithelial cells Epithelial-Mesenchymal Transition - genetics Epithelial-Mesenchymal Transition - physiology Epithelium Fibrosis Glycosaminoglycans Growth factors Homeostasis Humans Hypoxia Idiopathic Pulmonary Fibrosis - etiology Idiopathic Pulmonary Fibrosis - genetics Idiopathic Pulmonary Fibrosis - metabolism Inflammation - genetics Inflammation - metabolism Life Sciences Lung - metabolism Lung - pathology Lung diseases Lungs Mesenchyme Mitochondria Molecular modelling Non-coding RNA Oxidative stress Phenotypes pneumonia Polyadenylation Pulmonary fibrosis Review Risk analysis Risk Factors Senescence Smoking - adverse effects Unfolded Protein Response - genetics Unfolded Protein Response - physiology |
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| Title | Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis |
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