Lung remodeling mechanisms in chronic lung diseases

Zhong, Jun; Roth, Michael

doi:10.1097/aci.0000000000000022

Cited by 5 publications

(3 citation statements)

References 51 publications

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“…If failed, lung remodeling will happen which is very likely to result in harmful changes [14]. Pathological lung remodeling includes stressed or injured epithelium, increased smooth muscle mass, sub-epithelial fibrosis, goblet cell and sub-mucosal gland enlargement, hyperemia with increased vascularity of sub-epithelial tissues, thickening of basement membrane and extracellular matrix deposition [15, 16]. Airway remodeling appears in various chronic pulmonary disorders such as chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis and especially adult asthma [15].…”

Section: Introductionmentioning

confidence: 99%

“…Pathological lung remodeling includes stressed or injured epithelium, increased smooth muscle mass, sub-epithelial fibrosis, goblet cell and sub-mucosal gland enlargement, hyperemia with increased vascularity of sub-epithelial tissues, thickening of basement membrane and extracellular matrix deposition [15, 16]. Airway remodeling appears in various chronic pulmonary disorders such as chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis and especially adult asthma [15]. So far, mounting reports indicate that it is also common and early present in at least the moderate and severe type of pediatric asthma (2–15 years old) [17–20].…”

Section: Introductionmentioning

confidence: 99%

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Pleiotropic microRNA-21 in pulmonary remodeling: novel insights for molecular mechanism and present advancements

Jiang

Guo

et al. 2019

Allergy Asthma Clin Immunol

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MicroRNA-21 (miR-21), probably one of the most studied miRNAs to date, is found pleiotropic in various biological events. Its emerging role in pulmonary remodeling has attracted extensive attention. This review summarizes the genomic information of its primary transcript and various transcriptional regulations on its promoter. In addition, the role of miR-21 in pulmonary remodeling related signaling such as transforming growth factor β (TGF-β), bone morphogenetic protein (BMP), epidermal growth factor receptor (EGFR) and Notch signaling is discussed. Various validated miR-21 target genes participate in controlling of the overactive cell accumulation, smooth muscle contraction, inflammatory stress (trigger for lung epithelium damage), extracellular matrix deposition and hypoxia-induced disorders. Moreover, we focus on its particular implication in events including inflammatory stress-driven epithelium damage, epithelial-to-mesenchymal transition (EMT), transdifferentiation of fibroblasts into myofibroblasts, hypoxia stimuli and ROS response, as well as some other pulmonary remodeling related events such as overactive fibroblast (myofibroblast) accumulation, extracellular matrix deposition, and angiogenesis. Here, we summarize the strong potential of miR-21 in pulmonary remodeling and provide novel clues for further research in this area.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pleiotropic microRNA-21 in pulmonary remodeling: novel insights for molecular mechanism and present advancements

Jiang

Guo

et al. 2019

Allergy Asthma Clin Immunol

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“…Given that lung late effects (fibrosis) and regulatory T cell differentiation share common signaling pathways, and that regulatory T cells play a role in the resolution of inflammation after viral clearance, we assessed the frequency of regulatory T cells in the lymph nodes that drain the lung (15–18). Due to animal number limitations, we were only able to harvest mediastinal lymph nodes from mice that were externally irradiated 26 weeks earlier.…”

Section: Resultsmentioning

confidence: 99%

Examining the Effects of External or Internal Radiation Exposure of Juvenile Mice on Late Morbidity after Infection with Influenza A

et al. 2015

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A number of investigators have suggested that exposure to low-dose radiation may pose a potentially serious health risk. However, the majority of these studies have focused on the short-term rather than long-term effects of exposure to fixed source radiation, and few have examined the effects of internal contamination. Additionally, very few studies have focused on exposure in juveniles, when organs are still developing and could be more sensitive to the toxic effects of radiation. To specifically address whether early-life radiation injury may affect long-term immune competence, we studied 14-day-old juvenile pups that were either 5 Gy total-body irradiated or injected internally with 50 μCi soluble 137Cs, then infected with influenza A virus at 26 weeks after exposure. After influenza infection, all groups demonstrated immediate weight loss. We found that externally irradiated, infected animals failed to recover weight relative to age-matched infected controls, but internally 137Cs contaminated and infected animals had a weight recovery with a similar rate and degree as controls. Externally and internally irradiated mice demonstrated reduced levels of club cell secretory protein (CCSP) message in their lungs after influenza infection. The externally irradiated group did not recover CCSP expression even at the two-week time point after infection. Although the antibody response and viral titers did not appear to be affected by either radiation modality, there was a slight increase in monocyte chemo-attractant protein (MCP)-1 expression in the lungs of externally irradiated animals 14 days after influenza infection, with increased cellular infiltration present. Notably, an increase in the number of regulatory T cells was seen in the mediastinal lymph nodes of irradiated mice relative to uninfected mice. These data confirm the hypothesis that early-life irradiation may have long-term consequences on the immune system, leading to an altered antiviral response.

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Strategies for identifying pulmonary sarcoidosis patients at risk for severe or chronic disease

Judson

2017

Expert Review of Respiratory Medicine

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Most of the morbidity and mortality resulting from pulmonary sarcoidosis relates to complications of fibrotic disease. Because the fibrosis related to pulmonary sarcoidosis is often of minimal clinical importance, pharmacotherapy is not mandated. However, a small fraction of pulmonary sarcoidosis patients develop significant lung fibrosis, and they could potentially benefit from anti-sarcoidosis therapy. A reliable algorithm to determine the likelihood of a pulmonary sarcoidosis patient developing fibrosis would minimize the toxicity of therapy and potentially prevent serious complications of the disease. Areas covered: The mechanisms of fibrosis in pulmonary sarcoidosis are discussed. Granulomatous inflammation is the major cause of fibrosis in pulmonary sarcoidosis. Known risk factors for the development of persistent and fibrotic sarcoidosis, including genetic risk factors are explored. Expert opinion/commentary: Currently, methods to determine the propensity of a pulmonary sarcoidosis to develop significant fibrosis are unreliable. This is an important unmet medical need.

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Lung remodeling mechanisms in chronic lung diseases

Cited by 5 publications

References 51 publications

Pleiotropic microRNA-21 in pulmonary remodeling: novel insights for molecular mechanism and present advancements

Pleiotropic microRNA-21 in pulmonary remodeling: novel insights for molecular mechanism and present advancements

Examining the Effects of External or Internal Radiation Exposure of Juvenile Mice on Late Morbidity after Infection with Influenza A

Strategies for identifying pulmonary sarcoidosis patients at risk for severe or chronic disease

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