-
Radiology Aug 2020
Topics: Aged; Humans; Imaging, Three-Dimensional; Lung; Male; Pulmonary Emphysema; Pulmonary Fibrosis; Tomography, X-Ray Computed
PubMed: 32368964
DOI: 10.1148/radiol.2020200130 -
Cells Aug 2022Pulmonary fibrosis (PF) is a feared outcome of many pulmonary diseases which results in a reduction in lung compliance and capacity. The development of PF is relatively... (Review)
Review
Pulmonary fibrosis (PF) is a feared outcome of many pulmonary diseases which results in a reduction in lung compliance and capacity. The development of PF is relatively rare, but it can occur secondary to viral pneumonia, especially COVID-19 infection. While COVID-19 infection and its complications are still under investigation, we can look at a similar outbreak in the past to gain better insight as to the expected long-term outcomes of COVID-19 patient lung function. In the current article, we review the literature relative to PF via PubMed. We also performed a literature search for COVID-related pathological changes in the lungs. Finally, the paper was reviewed and summarized based on the studies' integrity, relative, or power calculations. This article provides a narrative review that endeavors to elucidate the current understanding of the pathophysiological mechanisms underlying PF and therapeutic strategies. We also discussed the potential for preventing progression to the fibrotic state within the context of the COVID-19 pandemic. With the massive scale of the COVID-19 pandemic, we expect there should more instances of PF due to COVID-19 infection. Patients who survive severe COVID-19 infection may suffer from a high incidence of PF.
Topics: COVID-19; Humans; Lung; Pandemics; Pneumonia, Viral; Pulmonary Fibrosis
PubMed: 36010566
DOI: 10.3390/cells11162489 -
American Journal of Physiology. Lung... Sep 2020
Topics: Awareness; Biomedical Research; Humans; Idiopathic Pulmonary Fibrosis; Pulmonary Fibrosis
PubMed: 32755301
DOI: 10.1152/ajplung.00335.2020 -
Cancer Radiotherapie : Journal de La... Sep 2023Radiation-induced pulmonary fibrosis (RIPF) is one of the major and late complications of radiotherapy (RT) with an average incidence rate between 16 and 28% after RT.... (Review)
Review
Radiation-induced pulmonary fibrosis (RIPF) is one of the major and late complications of radiotherapy (RT) with an average incidence rate between 16 and 28% after RT. RIPF significantly affects the function of the affected tissues/organs as well as the quality of life and survival of patients. The process of radiation fibrogenesis is initiated by a very complex signaling network that involves several cellular and molecular factors and the development of effective treatments relies on a better understanding of the involved mechanisms. Despite a major advance in the field, to date there is no clinical treatment that has really shown efficacy in the prevention or treatment of RIPF. In the present review, we will discuss potential new therapeutic avenues that could effectively treat RIPF.
Topics: Humans; Pulmonary Fibrosis; Quality of Life; Radiation Oncology; Signal Transduction
PubMed: 37596124
DOI: 10.1016/j.canrad.2023.06.026 -
International Journal of Molecular... May 2023The pathological features of pulmonary fibrosis (PF) are the abnormal activation and proliferation of myofibroblasts and the extraordinary deposition of the... (Review)
Review
The pathological features of pulmonary fibrosis (PF) are the abnormal activation and proliferation of myofibroblasts and the extraordinary deposition of the extracellular matrix (ECM). However, the pathogenesis of PF is still indistinct. In recent years, many researchers have realized that endothelial cells had a crucial role in the development of PF. Studies have demonstrated that about 16% of the fibroblasts in the lung tissue of fibrotic mice were derived from endothelial cells. Endothelial cells transdifferentiated into mesenchymal cells via the endothelial-mesenchymal transition (E(nd)MT), leading to the excessive proliferation of endothelial-derived mesenchymal cells and the accumulation of fibroblasts and ECM. This suggested that endothelial cells, a significant component of the vascular barrier, played an essential role in PF. Herein, this review discusses E(nd)MT and its contribution to the activation of other cells in PF, which could provide new ideas for further understanding the source and activation mechanism of fibroblasts and the pathogenesis of PF.
Topics: Mice; Animals; Pulmonary Fibrosis; Endothelial Cells; Fibrosis; Fibroblasts; Myofibroblasts; Risk Factors
PubMed: 37240093
DOI: 10.3390/ijms24108749 -
Translational Research : the Journal of... Dec 2018Idiopathic pulmonary fibrosis (IPF) and other forms of lung fibrosis are age-associated diseases with increased deposition of mesenchymal collagen that promotes... (Review)
Review
Idiopathic pulmonary fibrosis (IPF) and other forms of lung fibrosis are age-associated diseases with increased deposition of mesenchymal collagen that promotes respiratory malfunction and eventual death from respiratory failure. Our understanding of the pathobiology underlying pulmonary fibrosis is incomplete and current therapies available to slow or treat lung fibrosis are limited. Evidence reviewed herein demonstrates key involvement of mitochondrial dysfunction in diverse pulmonary cell populations, including alveolar epithelial cells (AEC), fibroblasts, and macrophages and/or immune cells that collectively advances the development of pulmonary fibrosis. The mitochondria have an important role in regulating whether fibrogenic stimuli results in the return of normal healthy function ("friend") or the development of pulmonary fibrosis ("foe"). In particular, we summarize the evidence suggesting that AEC mitochondrial dysfunction is important in mediating lung fibrosis signaling via mechanisms involving imbalances in the levels of reactive oxygen species, endoplasmic reticulum stress response, mitophagy, apoptosis and/or senescence, and inflammatory signaling. Further, we review the emerging evidence suggesting that dysfunctional mitochondria in AECs and other cell types play crucial roles in modulating nearly all aspects of the 9 hallmarks of aging in the context of pulmonary fibrosis as well as some novel molecular pathways that have recently been identified. Finally, we discuss the potential translational aspects of these studies as well as the key knowledge gaps necessary for better informing our understanding of the pathobiology of the mitochondria in mediating pulmonary fibrosis. We reason that targeting deficient mitochondria-derived pathways may provide innovative future treatment strategies that are urgently needed for lung fibrosis.
Topics: Animals; Apoptosis; DNA Damage; Endoplasmic Reticulum Stress; Humans; Mitochondria; Pulmonary Fibrosis; Reactive Oxygen Species
PubMed: 30036495
DOI: 10.1016/j.trsl.2018.05.005 -
Current Opinion in Pulmonary Medicine Jul 2017The pathogenesis of lung cancer and pulmonary fibrotic disorders partially overlaps. This review focuses on the common features of the two disease categories, aimed at... (Review)
Review
PURPOSE OF REVIEW
The pathogenesis of lung cancer and pulmonary fibrotic disorders partially overlaps. This review focuses on the common features of the two disease categories, aimed at advancing our translational understanding of their pathobiology and at fostering the development of new therapies.
RECENT FINDINGS
Both malignant and collagen-producing lung cells display enhanced cellular proliferation, increased resistance to apoptosis, a propensity for invading and distorting the lung parenchyma, as well as stemness potential. These characteristics are reinforced by the tissue microenvironment and inflammation seems to play an important adjuvant role in both types of disorders.
SUMMARY
Unraveling the thread of the common and distinct characteristics of lung fibrosis and cancer might contribute to a more comprehensive approach of the pathobiology of both diseases and to a pathfinder for novel and personalized therapeutic strategies.
Topics: Aging; Apoptosis; Carcinogenesis; Humans; Lung Neoplasms; Pulmonary Fibrosis
PubMed: 28403038
DOI: 10.1097/MCP.0000000000000390 -
Chest May 2017This review addresses common questions regarding the role of surgical lung biopsy (SLB) in the diagnosis and treatment of interstitial lung disease (ILD). We... (Review)
Review
This review addresses common questions regarding the role of surgical lung biopsy (SLB) in the diagnosis and treatment of interstitial lung disease (ILD). We specifically address when a SLB can be diagnostic as well as when it may be avoided; for example, when the combination of the clinical context and the imaging pattern seen on high-resolution CT (HRCT) chest scans can provide a confident diagnosis. Existing studies on the diagnostic utility as well as the complications associated with SLB are reviewed; also reviewed are the performance characteristics and reliability of HRCT scans of the chest in predicting the underlying histopathologic findings of the lung. The review is formatted in the form of answers to questions that clinicians regularly ask when considering an SLB in a patient with ILD.
Topics: Alveolitis, Extrinsic Allergic; Biopsy; Bronchoscopy; Humans; Idiopathic Pulmonary Fibrosis; Lung; Lung Diseases, Interstitial; Pulmonary Fibrosis; Thoracic Surgical Procedures; Tomography, X-Ray Computed
PubMed: 27471113
DOI: 10.1016/j.chest.2016.06.019 -
European Journal of Pharmacology Oct 2023Pulmonary fibrosis is a chronic and progressive fibrotic disease that results in impaired gas exchange, ventilation, and eventual death. The pro-fibrotic environment is... (Review)
Review
Pulmonary fibrosis is a chronic and progressive fibrotic disease that results in impaired gas exchange, ventilation, and eventual death. The pro-fibrotic environment is instigated by various factors, leading to the transformation of epithelial cells into myofibroblasts and/or fibroblasts that trigger fibrosis. Epithelial mesenchymal transition (EMT) is a biological process that plays a critical role in the pathogenesis of pulmonary fibrosis. Epigenetic regulation of tissue-stromal crosstalk involving DNA methylation, histone modifications, non-coding RNA, and chromatin remodeling plays a key role in the control of EMT. The review investigates the epigenetic regulation of EMT and its significance in pulmonary fibrosis.
Topics: Humans; Pulmonary Fibrosis; Epithelial-Mesenchymal Transition; Epigenesis, Genetic; Lung; Fibrosis
PubMed: 37541361
DOI: 10.1016/j.ejphar.2023.175959 -
Naunyn-Schmiedeberg's Archives of... Jun 2023Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease that is characterized by abnormal proliferation of fibroblasts and extracellular matrix...
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease that is characterized by abnormal proliferation of fibroblasts and extracellular matrix remodeling, ultimately leading to respiratory insufficiency or even death. Naringin (Nar), a natural compound derived from grapefruit and citrus fruits, has several pharmacological activities that are associated with therapeutic benefits for IPF. However, the specific molecular mechanisms underlying its pulmonary tissue-protective effects remain largely unknown. This study aimed to investigate the effects of Nar on endoplasmic reticulum stress (ERS) and mitophagy. A bleomycin (BLM)-induced mouse model of IPF was established for treatment with different doses of Nar. Histopathological changes in the lung were examined by hematoxylin and eosin (HE) staining and Masson staining. The extent of fibrosis was determined by measuring hydroxyproline and collagen expression levels. The levels of inflammatory cytokines and oxidative stress indicators were determined by Enzyme linked immunosorbent assay (ELISA) and biochemical kits. Western blot and immunofluorescence were used to evaluate the expression levels of the mitophagy-related markers. Cell apoptosis was estimated by western blot and TUNEL staining. Nar reduced the levels of inflammatory response, oxidative stress and decreased the proportion of apoptosis. Nar also inhibited the expression of the ERS and mitophagy-related genes and ERS-downstream proteins, thereby activating transcription factor (ATF) 3 and inhibiting the transcription of PTEN-induced kinase 1 (PINK1). Taken together, Nar is a promising therapeutic agent for treating IPF via inhibiting ERS, reducing apoptosis, and maintaining mitochondrial homeostasis, all of which may be associated with the regulation of the ATF3/PINK1 signaling axis.
Topics: Mice; Animals; Pulmonary Fibrosis; Mitophagy; Protein Kinases; Endoplasmic Reticulum Stress; Bleomycin
PubMed: 36688958
DOI: 10.1007/s00210-023-02390-z