Pulmonary fibrosis, part I: epidemiology, pathogenesis, and diagnosis

Meyer, Keith C.

doi:10.1080/17476348.2017.1312346

Cited by 140 publications

(141 citation statements)

References 165 publications

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“…Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease with high lethality, a fatal prognosis, and a lack of effective medical therapies [ 1 , 2 ]. The pathological characteristics of IPF mainly include the disruption of the pulmonary parenchymal matrix and replacement with fibrotic tissues [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

Gefitinib Inhibits Bleomycin‐Induced Pulmonary Fibrosis via Alleviating the Oxidative Damage in Mice

Cai

Zheng

et al. 2018

Oxidative Medicine and Cellular Longevity

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Pulmonary fibrosis (PF) is a life-threatening interstitial lung disease. In this study, we tried to reveal the model of action between high-mobility group box 1 (HMGB1) and α-smooth muscle actin (α-SMA) and the protective role of gefitinib in pulmonary fibrosis induced by the administration of bleomycin aerosol in mice. For the mechanism study, lung tissues were harvested two weeks after modeling to detect the coexpression of HMGB1 and α-SMA by immunohistochemistry and immunofluorescence staining. Protein-DNA interactions were analyzed using a pulldown assay to study the relationship between HMGB1 and α-SMA. For the gefitinib treatment study, the mice were divided into three groups: phosphate-buffered saline (PBS) control group, PBS-treated PF group, and gefitinib-treated PF group. Gavage of gefitinib or PBS (20 mg/kg/day) was performed after bleomycin treatment for two weeks until the mice were sacrificed. Lung and blood samples were collected to assess the histological changes, oxidative stress, and expression of NOXs, HMGB1, EGFR, MAPKs, AP-1, and NF-κB to determine the curative effect and related molecular mechanisms. The results revealed the high coexpression of α-SMA and HMGB1 in some interstitial cells in the fibrotic lung. The DNA-protein pulldown analysis proved that HMGB34367 acted as a novel transcriptional factor for the α-SMA promoter and participated in the eventual development of pulmonary fibrosis. Second, gefitinib could significantly decrease lung fibrotic changes and the level of MDA and recover the T-AOC level. Meanwhile, gefitinib could also reduce the NOX1/2/4, HMGB1, p-EGFR, p-ERK, p-JNK, p-P38, p-NF-κB, p-c-Jun, and p-c-Fos expression levels in fibrotic lungs. The present study suggested that gefitinib could alleviate lung fibrosis through the HMGB1/NOXs-ROS/EGFR-MAPKs-AP-1/NF-κB signal in bleomycin-induced pulmonary fibrosis.

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Section: Introductionmentioning

confidence: 99%

Gefitinib Inhibits Bleomycin‐Induced Pulmonary Fibrosis via Alleviating the Oxidative Damage in Mice

Cai

Zheng

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…Early studies that identified evidence of inherited risk for developing pulmonary fibrosis focused on familial cases, including variants such as genes coding for mucin 5B surfactant proteins [136] or those involved in telomere homeostasis and function [73]. Studies that have focused particularly on genome-wide linkage analyses have identified numerous gene polymorphisms that are associated with increased risk for pulmonary fibrosis [135,[138][139][140]. However, not all races have been evaluated, even for widely studied genetic mutations that have demonstrated their association with pulmonary fibrosis.…”

Section: Genetics Of Pulmonary Fibrosismentioning

confidence: 99%

Interstitial Lung Diseases in Developing Countries

Ortega

Molina-Molina

2019

Annals of Global Health

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More than 100 different conditions are grouped under the term interstitial lung disease (ILD). A diagnosis of an ILD primarily relies on a combination of clinical, radiological, and pathological criteria, which should be evaluated by a multidisciplinary team of specialists. Multiple factors, such as environmental and occupational exposures, infections, drugs, radiation, and genetic predisposition have been implicated in the pathogenesis of these conditions. Asbestosis and other pneumoconiosis, hypersensitivity pneumonitis (HP), chronic beryllium disease, and smoking-related ILD are specifically linked to inhalational exposure of environmental agents. The recent Global Burden of Disease Study reported that ILD rank 40th in relation to global years of life lost in 2013, which represents an increase of 86% compared to 1990. Idiopathic pulmonary fibrosis (IPF) is the prototype of fibrotic ILD. A recent study from the United States reported that the incidence and prevalence of IPF are 14.6 per 100,000 person-years and 58.7 per 100,000 persons, respectively. These data suggests that, in large populated areas such as Brazil, Russia, India, and China (the BRIC region), there may be approximately 2 million people living with IPF. However, studies from South America found much lower rates (0.4-1.2 cases per 100,000 per year). Limited access to highresolution computed tomography and spirometry or to multidisciplinary teams for accurate diagnosis and optimal treatment are common challenges to the management of ILD in developing countries.

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“…In humans, 28 types of collagens have been identi ed, and more than 1300 mutations in collagen-associated genes are linked with genetic diseases 4,6 . As with the ECM de ciency problem, excessive secretion and accumulation of ECM causes serious brotic diseases such as liver, kidney, heart and lung brosis 7,8,9 . Fibrosis that forms in solid cancer tissue is necessary or accelerated for cancer growth and metastasis 5 .…”

Section: Introductionmentioning

confidence: 99%

SURO-2/TMEM39 Facilitates Collagen Secretion through the Formation of Large COPII Vesicles

Lee

Sung²,

Lee³

et al. 2020

Preprint

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Fibrosis of various tissues is a typical disease caused by excessive production and secretion of extracellular matrix. We used Caenorhabditis elegans to investigate the formation of large transport vesicles to understand collagen secretion, a critical factor in fibrosis formation. The suro-2 mutant displays obvious defects in collagen secretion and cuticle structure including a rupture phenotype in early adults. Transmission electron microscopy exhibited that the cuticle thickness of the suro-2 mutant was severely reduced. SURO-2/TMEM39 has 8 transmembrane domains and localizes in the endoplasmic reticulum (ER) membrane. SURO-2 interacts directly with NPP-20/Sec13, a component of the coat protein II (COPII) complex responsible for ER-to-Golgi transport. SURO-2 and NPP-20 localized at the same large puncta, a large COPII vesicle enough to accommodate collagens. We report here that SURO-2/TMEM39 is highly conserved among animal species and is a specialized regulator of bulky collagen secretion rather than general transport in C. elegans.

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Pulmonary fibrosis, part I: epidemiology, pathogenesis, and diagnosis

Cited by 140 publications

References 165 publications

Gefitinib Inhibits Bleomycin‐Induced Pulmonary Fibrosis via Alleviating the Oxidative Damage in Mice

Gefitinib Inhibits Bleomycin‐Induced Pulmonary Fibrosis via Alleviating the Oxidative Damage in Mice

Interstitial Lung Diseases in Developing Countries

SURO-2/TMEM39 Facilitates Collagen Secretion through the Formation of Large COPII Vesicles

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