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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 -
Frontiers in Immunology 2023Post-acute COVID-19 sequelae, commonly known as long COVID, encompasses a range of systemic symptoms experienced by a significant number of COVID-19 survivors. The... (Review)
Review
Post-acute COVID-19 sequelae, commonly known as long COVID, encompasses a range of systemic symptoms experienced by a significant number of COVID-19 survivors. The underlying pathophysiology of long COVID has become a topic of intense research discussion. While chronic inflammation in long COVID has received considerable attention, the role of neutrophils, which are the most abundant of all immune cells and primary responders to inflammation, has been unfortunately overlooked, perhaps due to their short lifespan. In this review, we discuss the emerging role of neutrophil extracellular traps (NETs) in the persistent inflammatory response observed in long COVID patients. We present early evidence linking the persistence of NETs to pulmonary fibrosis, cardiovascular abnormalities, and neurological dysfunction in long COVID. Several uncertainties require investigation in future studies. These include the mechanisms by which SARS-CoV-2 brings about sustained neutrophil activation phenotypes after infection resolution; whether the heterogeneity of neutrophils seen in acute SARS-CoV-2 infection persists into the chronic phase; whether the presence of autoantibodies in long COVID can induce NETs and protect them from degradation; whether NETs exert differential, organ-specific effects; specifically which NET components contribute to organ-specific pathologies, such as pulmonary fibrosis; and whether senescent cells can drive NET formation through their pro-inflammatory secretome in long COVID. Answering these questions may pave the way for the development of clinically applicable strategies targeting NETs, providing relief for this emerging health crisis.
Topics: Humans; Extracellular Traps; COVID-19; Post-Acute COVID-19 Syndrome; SARS-CoV-2; Pulmonary Fibrosis; Inflammation
PubMed: 37828990
DOI: 10.3389/fimmu.2023.1254310 -
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 -
American Journal of Respiratory Cell... Aug 2023Lungs are constantly exposed to environmental perturbations and therefore have remarkable capacity to regenerate in response to injury. Sustained lung injuries, aging,... (Review)
Review
Lungs are constantly exposed to environmental perturbations and therefore have remarkable capacity to regenerate in response to injury. Sustained lung injuries, aging, and increased genomic instability, however, make lungs particularly susceptible to disrepair and fibrosis. Pulmonary fibrosis constitutes a major cause of morbidity and is often relentlessly progressive, leading to death from respiratory failure. The pulmonary vasculature, which is critical for gas exchanges and plays a key role during lung development, repair, and regeneration, becomes aberrantly remodeled in patients with progressive pulmonary fibrosis. Although capillary rarefaction and increased vascular permeability are recognized as distinctive features of fibrotic lungs, the role of vasculature dysfunction in the pathogenesis of pulmonary fibrosis has only recently emerged as an important contributor to the progression of this disease. This review summarizes current findings related to lung vascular repair and regeneration and provides recent insights into the vascular abnormalities associated with the development of persistent lung fibrosis.
Topics: Humans; Pulmonary Fibrosis; Lung; Fibrosis; Lung Injury; Respiratory Insufficiency; Idiopathic Pulmonary Fibrosis
PubMed: 37126595
DOI: 10.1165/rcmb.2022-0431TR -
Molecular Therapy : the Journal of the... Oct 2023Pirfenidone and nintedanib are only anti-pulmonary fibrosis (PF) drugs approved by the FDA. However, they are not target specific, and unable to modify the disease...
Pirfenidone and nintedanib are only anti-pulmonary fibrosis (PF) drugs approved by the FDA. However, they are not target specific, and unable to modify the disease status. Therefore, it is still desirable to discover more effective agents against PF. Vimentin (VIM) plays key roles in tissue regeneration and wound healing, but its molecular mechanism remains unknown. In this work, we demonstrated that atractylodinol (ATD) significantly inhibits TGF-β1-induced epithelial-mesenchymal transition and fibroblast-to-myofibroblast transition in vitro. ATD also reduces bleomycin-induced lung injury and fibrosis in mice models. Mechanistically, ATD inhibited TGF-β receptor I recycling by binding to VIM (K = 454 nM) and inducing the formation of filamentous aggregates. In conclusion, we proved that ATD (derived from Atractylodes lancea) modified PF by targeting VIM and inhibiting the TGF-β/Smad signaling pathway. Therefore, VIM is a druggable target and ATD is a proper drug candidate against PF. We prove a novel VIM function that TGF-β receptor I recycling. These findings paved the way to develop new targeted therapeutics against PF.
Topics: Animals; Mice; Bleomycin; Epithelial-Mesenchymal Transition; Lung; Pulmonary Fibrosis; Receptor, Transforming Growth Factor-beta Type I; Transforming Growth Factor beta1; Vimentin
PubMed: 37641404
DOI: 10.1016/j.ymthe.2023.08.017 -
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