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Bioorganic Chemistry Sep 2023Pulmonary fibrosis is the end-stage change of a large class of lung diseases characterized by the proliferation of fibroblasts and the accumulation of a large amount of... (Review)
Review
Pulmonary fibrosis is the end-stage change of a large class of lung diseases characterized by the proliferation of fibroblasts and the accumulation of a large amount of extracellular matrix, accompanied by inflammatory damage and tissue structure destruction, which also shows the normal alveolar tissue is damaged and then abnormally repaired resulting in structural abnormalities (scarring). Pulmonary fibrosis has a serious impact on the respiratory function of the human body, and the clinical manifestation is progressive dyspnea. The incidence of pulmonary fibrosis-related diseases is increasing year by year, and no curative drugs have appeared so far. Nevertheless, research on pulmonary fibrosis have also increased in recent years, but there are no breakthrough results. Pathological changes of pulmonary fibrosis appear in the lungs of patients with coronavirus disease 2019 (COVID-19) that have not yet ended, and whether to improve the condition of patients with COVID-19 by means of the anti-fibrosis therapy, which are the questions we need to address now. This review systematically sheds light on the current state of research on fibrosis from multiple perspectives, hoping to provide some references for design and optimization of subsequent drugs and the selection of anti-fibrosis treatment plans and strategies.
Topics: Humans; Pulmonary Fibrosis; COVID-19; Lung; Fibrosis; Fibroblasts
PubMed: 37178650
DOI: 10.1016/j.bioorg.2023.106592 -
Respirology (Carlton, Vic.) Mar 2022
Topics: Alveolitis, Extrinsic Allergic; Humans; Pulmonary Fibrosis
PubMed: 35146840
DOI: 10.1111/resp.14225 -
QJM : Monthly Journal of the... Nov 2021
Topics: COVID-19; Humans; Lung; Pulmonary Fibrosis; SARS-CoV-2
PubMed: 34002238
DOI: 10.1093/qjmed/hcab121 -
Archivos de Bronconeumologia Apr 2022
Topics: COVID-19; Humans; Lung; Pulmonary Fibrosis; Tomography, X-Ray Computed
PubMed: 35491285
DOI: 10.1016/j.arbres.2022.03.007 -
Therapeutische Umschau. Revue... Feb 2024Progressive pulmonary Fibrosis Abstract: Cough and dyspnea on excertion are common and early symptoms of interstitial lung diseases (ILD). Thoracic imaging (particularly... (Review)
Review
Progressive pulmonary Fibrosis Abstract: Cough and dyspnea on excertion are common and early symptoms of interstitial lung diseases (ILD). Thoracic imaging (particularly computed tomography) detects such lung structural alterations early in the disease course. Knowledge of these diseases and their management is necessary in the daily business. The term "progressive pulmonary fibrosis" subsumes a heterogene group of interstitial lung diseases with a similar course of progressive fibrosis. The management of these diseases should be discussed interdisciplinary, similar to the management of the Idiopathic pulmonary fibrosis (IPF). Antifibrotic drugs are new therapeutic options.
Topics: Humans; Antifibrotic Agents; Cough; Diagnosis, Differential; Disease Progression; Dyspnea; Idiopathic Pulmonary Fibrosis; Interdisciplinary Communication; Intersectoral Collaboration; Lung; Lung Diseases, Interstitial; Prognosis; Pulmonary Fibrosis; Tomography, X-Ray Computed
PubMed: 38655828
DOI: No ID Found -
Clinics in Chest Medicine Jun 2021Progress in the past 2 decades has led to widespread use of 2 medications to slow loss of lung function in patients with pulmonary fibrosis. Treatment of individual... (Review)
Review
Progress in the past 2 decades has led to widespread use of 2 medications to slow loss of lung function in patients with pulmonary fibrosis. Treatment of individual patients with currently available pharmacotherapies can be limited by side effects, and neither drug has a consistent effect on patient symptoms or function. Several promising new pharmacotherapies are under development. Comprehensive management of pulmonary fibrosis hinges on shared decision making. Patient and caregiver education, and early identification and management of symptoms and comorbidities, can help improve quality of life.
Topics: Comorbidity; Humans; Idiopathic Pulmonary Fibrosis; Quality of Life
PubMed: 34024403
DOI: 10.1016/j.ccm.2021.03.004 -
British Journal of Pharmacology Dec 2023Nitazoxanide is a therapeutic anthelmintic drug. Our previous studies found that nitazoxanide and its metabolite tizoxanide activated adenosine...
BACKGROUND AND PURPOSE
Nitazoxanide is a therapeutic anthelmintic drug. Our previous studies found that nitazoxanide and its metabolite tizoxanide activated adenosine 5'-monophosphate-activated protein kinase (AMPK) and inhibited signal transducer and activator of transcription 3 (STAT3) signals. As AMPK activation and/or STAT3 inhibition are targets for treating pulmonary fibrosis, we hypothesized that nitazoxanide would be effective in experimental pulmonary fibrosis.
EXPERIMENTAL APPROACH
The mitochondrial oxygen consumption rate of cells was measured by using the high-resolution respirometry system Oxygraph-2K. The mitochondrial membrane potential of cells was evaluated by tetramethyl rhodamine methyl ester (TMRM) staining. The target protein levels were measured by using western blotting. The mice pulmonary fibrosis model was established through intratracheal instillation of bleomycin. The examination of the lung tissues changes were carried out using haematoxylin and eosin (H&E), and Masson staining.
KEY RESULTS
Nitazoxanide and tizoxanide activated AMPK and inhibited STAT3 signalling in human lung fibroblast cells (MRC-5 cells). Nitazoxanide and tizoxanide inhibited transforming growth factor-β1 (TGF-β1)-induced proliferation and migration of MRC-5 cells, collagen-I and α-smooth muscle cell actin (α-SMA) expression, and collagen-I secretion from MRC-5 cells. Nitazoxanide and tizoxanide inhibited epithelial-mesenchymal transition (EMT) and inhibited TGF-β1-induced Smad2/3 activation in mouse lung epithelial cells (MLE-12 cells). Oral administration of nitazoxanide reduced the bleomycin-induced mice pulmonary fibrosis and, in the established bleomycin-induced mice, pulmonary fibrosis. Delayed nitazoxanide treatment attenuated the fibrosis progression.
CONCLUSIONS AND IMPLICATIONS
Nitazoxanide improves the bleomycin-induced pulmonary fibrosis in mice, suggesting a potential application of nitazoxanide for pulmonary fibrosis treatment in the clinic.
Topics: Humans; Mice; Animals; Pulmonary Fibrosis; Transforming Growth Factor beta1; AMP-Activated Protein Kinases; Bleomycin; Collagen Type I; Disease Models, Animal; Anthelmintics; Mice, Inbred C57BL; Nitro Compounds; Thiazoles
PubMed: 37428102
DOI: 10.1111/bph.16190 -
Archivos de Bronconeumologia May 2017
Topics: Forced Expiratory Volume; Humans; Pulmonary Emphysema; Pulmonary Fibrosis; Risk Factors; Smoking
PubMed: 28343743
DOI: 10.1016/j.arbres.2017.02.003 -
Acta Medica Indonesiana Apr 2021Pulmonary fibrosis due to COVID-19 is recognized as sequel of ARDS characterized by failed alveolar re-epithelization, fibroblast activation, excessive collagen... (Review)
Review
Pulmonary fibrosis due to COVID-19 is recognized as sequel of ARDS characterized by failed alveolar re-epithelization, fibroblast activation, excessive collagen deposition and other extracellular matrix components that disrupt the normal lung architecture. There are risk factor for pulmonary fibrosis namely advanced age, severe ARDS infection, mechanical ventilation due to ventilator-induced lung injury, smoking and chronic alcoholism. Diagnosis of post-COVID pulmonary fibrosis can be made by clinical symptoms and characteristic finding from lung CT scan. To date, there is no definitive treatment for post-inflammatory pulmonary fibrosis after COVID-19 infection, however some of antifibrotic therapies may be considered. Beside medical treatment, pulmonary rehabilitation program and long-term oxygen treatment should be included as part of comprehensive treatment for pulmonary fibrosis due to COVID-19.
Topics: COVID-19; Combined Modality Therapy; Humans; Pneumonia, Viral; Pulmonary Fibrosis; Risk Factors; SARS-CoV-2; Tomography, X-Ray Computed
PubMed: 34251354
DOI: No ID Found -
Clinics in Chest Medicine Jun 2021Fibrotic hypersensitivity pneumonitis (fHP) is a chronic, often progressive fibrosing form of interstitial lung disease caused by inhaled antigenic exposures. fHP can... (Review)
Review
Fibrotic hypersensitivity pneumonitis (fHP) is a chronic, often progressive fibrosing form of interstitial lung disease caused by inhaled antigenic exposures. fHP can lead to impaired respiratory function, reduced disease-related quality of life, and early mortality. Management of fHP should start with exposure remediation where possible, with systemic immunosuppression and antifibrotic therapy considered in patients with symptomatic or progressive disease. Nonpharmacologic and supportive management should be offered and, in cases of treatment-resistant, progressive illness, lung transplant should be considered.
Topics: Alveolitis, Extrinsic Allergic; Humans; Pulmonary Fibrosis
PubMed: 34024406
DOI: 10.1016/j.ccm.2021.03.007