Fibroblast growth factor 10 protects against particulate matter-induced lung injury by inhibiting oxidative stress-mediated pyroptosis via the PI3K/Akt/Nrf2 signaling pathway

Liu, Li; Shi, Qiangqiang; Wang, Kankai; Qian, Yao; Zhou, Liqin; Bellusci, Savério; Chen, Chengshui; Dong, Nian

doi:10.1016/j.intimp.2022.109398

Cited by 15 publications

(9 citation statements)

References 51 publications

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“…after lung bud formation in FGF10 knockout mice, leading to severe impairment of lung delevopment. 4,24,25 P3 and P4 described here also had significant and ultimately lethal chILD related to developmental disorders, and the histologic findings are comparable to those in the animal model in Fgf10 knockout mice mentioned above. Three of the four patients described here also had PH.…”

Section: Discussionsupporting

confidence: 79%

“…In 12 individuals with haploinsufficiency for FGF10 , significantly reduced vital capacity and reduced Tiffeneau index were observed mimicking chronic restrictive and/or obstructive pulmonary disease 12 . It has been shown that inactivation of FGF10 reduces epithelial branching after lung bud formation in FGF10 knockout mice, leading to severe impairment of lung delevopment 4,24,25 . P3 and P4 described here also had significant and ultimately lethal chILD related to developmental disorders, and the histologic findings are comparable to those in the animal model in Fgf10 knockout mice mentioned above.…”

Section: Discussionsupporting

confidence: 72%

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Variants in FGF10 cause early onset of severe childhood interstitial lung disease: A detailed description of four affected children

Schütz

Schmidt

Schwerk

et al. 2023

Pediatric Pulmonology

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IntroductionFibroblast growth factor 10 (FGF10) is a signaling molecule with a well‐established role for lung branching morphogenesis. Rare heterozygous, deleterious variants in the FGF10 gene are known causes of the lacrimo‐auriculo‐dento‐digital (LADD) syndrome and aplasia of lacrimal and salivary glands. Previous studies indicate that pathogenic variants in FGF10 can cause childhood Interstitial Lung Disease (chILD) due to severe diffuse developmental disorders of the lung, but detailed reports on clinical presentation and follow‐up of affected children are lacking.MethodsWe describe four children with postnatal onset of chILD and heterozygous variants in FGF10, each detected by exome or whole genome sequencing.ResultsAll children presented with postnatal respiratory failure. Two children died within the first 2 days of life, one patient died at age of 12 years due to right heart failure related to severe pulmonary hypertension (PH) and one patient is alive at age of 6 years, but still symptomatic. Histopathological analysis of lung biopsies from the two children with early postpartum demise revealed diffuse developmental disorder representing acinar dysplasia and interstitial fibrosis. Sequential biopsies of the child with survival until the age of 12 years revealed alveolar simplification and progressive interstitial fibrosis.DiscussionOur report extends the phenotype of FGF10‐related disorders to early onset chILD with progressive interstitial lung fibrosis and PH. Therefore, FGF10‐related disorder should be considered even without previously described syndromic stigmata in children with postnatal respiratory distress, not only when leading to death in the neonatal period but also in case of persistent respiratory complaints and PH.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionsupporting

confidence: 72%

Variants in FGF10 cause early onset of severe childhood interstitial lung disease: A detailed description of four affected children

Schütz

Schmidt

Schwerk

et al. 2023

Pediatric Pulmonology

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“…The participation of the nuclear factor erythroid 2-related factor 2 (Nrf2) in the oxidative stress triggered by PM has been extensively reported in recent years (Badran et al, 2020;Bagam et al, 2021;Housseiny et al, 2020;Ito et al, 2020;Liu et al, 2022b;Saha et al, 2022;Shi et al, 2023;Shrestha et al, 2021;Son et al, 2020;Tian et al, 2021;Wang et al, 2022aWang et al, , 2022bWang et al, , 2022cXue et al, 2021b). This is not surprising given the key role of Nrf2 in the protection against oxidative stimuli (Saha et al, 2020), acting as a sensor to protect the cells against oxidative damage induced by PM-generated ROS.…”

Section: Nrf2: the Master Regulator Of Antioxidant Responsementioning

confidence: 96%

Particulate Matter-Induced Oxidative Stress – Recent Mechanistic Insights from In Vitro Studies

Vilas-Boas,

Chatterjee,

Carvalho

et al. 2024

Preprint

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Inhaled particulate matter (PM) is a key player in the millions of yearly deaths worldwide related to air pollution. The oxidative potential of PM provides an indication of its ability to promote an oxidative environment. When the human lungs are exposed to PM, the reactive oxygen species (ROS) generated in such oxidative environment, if excessive, may lead to cell damage via oxidative stress. Inflammation, endoplasmic reticulum stress, airway remodeling, and many different cell death modes (apoptosis, ferroptosis, pyroptosis, among others) can be triggered by oxidative stress via complex molecular pathways, which also involve the adaptive cellular response. But ROS can also directly interact with macromolecules such as proteins and lipids, as well as nucleic acids, having been reported to induce DNA damage and epigenetic modifications, which jeopardizes homeostasis. These facts have been extensively studied in in vitro models and confirmed in in vivo models.In this review, we delve beyond conventional assessments of airborne particles, discussing their oxidative potential and the PM-induced ROS-mediated cellular damage observed in in vitro models. The close link between oxidative stress and inflammation, and the manifestation of different cell death modes is highlighted by reviewing the latest literature. The effects of ROS on the balance of DNA damage and repair, carcinogenicity and epigenetics interplay are then analyzed. Finally, we expand on the latest reports on the antioxidants’ potential to counteract the deleterious effects of ROS, and disclose future perspectives for the topic.

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“…PM 2.5 induce the production of ROS through the NODlike receptor protein 3 (NLRP3) inflammasome, which triggers the activation of caspase-1 and the subsequent activation of IL-1β, which can cause airway inflammation (Borthwick, 2016;Xu et al, 2019;Jia et al, 2021;Liu et al, 2022aLiu et al, , 2022b. Exposure to PM 2.5 decreases miR-331 expression through the ROS/phosphoinositide 3-kinases/ Protein kinase B (ROS/PI3K/Akt) pathway, leading to the activation and increased expression of IκB kinase (IKK-β) and nuclear factor kappa B (NFκB) in human airway epithelial cells (Song et al, 2017).…”

Section: Asthmamentioning

confidence: 99%

“…Pyroptosis, a type of programmed cell death mediated by caspases-1 or -11, may play a crucial role in epithelial injury and airway remodeling, thereby aggravating or inducing asthma and COPD by TLR4/NF-κB pathway (Wang et al, 2022b). FGF10 inhibits oxidative stressmediated pyroptosis via the PI3K/Akt/Nrf2 pathway (Liu et al, 2022b;Wang et al, 2022). FIGURE 1.…”

Section: Chronic Obstructive Pulmonary Disease (Copd)mentioning

confidence: 99%

Molecular mechanisms and cellular process in signal transduction pathway related to air pollutants in obstructive lung diseases: A mini-review

JANG

2023

Biocell

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Exposure to air pollutants such as PM 10 , PM 2.5 , PM 0.1 , O 3 , CO, NO 2 , and SO 2 , and biological pollutants are important factors causing the evolution and furtherance of obstructive lung diseases (OLD), including asthma and chronic obstructive pulmonary disease (COPD). Asthma is the most frequent chronic inflammatory airway disease, characterized by breathlessness, wheezing, chest tightness, and cough, together with the presence of exaggerated expiratory airflow fluctuation that varies over time. COPD is a heterogeneous lung condition characterized by chronic respiratory symptoms such as dyspnea, cough, expectoration, and/or exacerbations due to abnormalities of the airways and/or alveoli that cause persistent, often progressive, airflow obstruction. Understanding the molecular mechanisms and cellular processes based on the development of OLD on exposure to air pollutants will provide insights into the solution of pathogenesis, prevention, and treatment of these conditions. The molecular mechanisms and cellular process involved in signal transduction pathway plays a role in the binding of extracellular signaling molecules and ligands to receptors placed on the cell surface or on the inner side cell that trigger inflammation that occurs, especially when something important enters the cell to bring into a cascade response. This binding then alters the cell metabolism, shape, and gene expression in the airway. This review aimed to reveal the effect of air pollutants on the molecular mechanisms and cellular processes involved in the signal transduction pathways in OLD.

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Fibroblast growth factor 10 protects against particulate matter-induced lung injury by inhibiting oxidative stress-mediated pyroptosis via the PI3K/Akt/Nrf2 signaling pathway

Cited by 15 publications

References 51 publications

Variants in FGF10 cause early onset of severe childhood interstitial lung disease: A detailed description of four affected children

Variants in FGF10 cause early onset of severe childhood interstitial lung disease: A detailed description of four affected children

Particulate Matter-Induced Oxidative Stress – Recent Mechanistic Insights from In Vitro Studies

Molecular mechanisms and cellular process in signal transduction pathway related to air pollutants in obstructive lung diseases: A mini-review

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