Oxidative Stress in Pulmonary Fibrosis

Otoupalova, Eva; Smith, S. Ray; Cheng, Guangjie; Thannickal, Victor J.

doi:10.1002/cphy.c190017

Cited by 133 publications

(71 citation statements)

References 617 publications

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“…Oxidative stress, an imbalance between oxidants and antioxidants, and inflammation also play important roles in the development and progression of pulmonary fibrosis (Cameli et al, 2020;Otoupalova et al, 2020). One study found that the levels of T-SOD, catalase (CAT), and glutathione (GSH) were significantly decreased, and the expressions of MDA were significantly increased in rat lung and serum after Blm treatment (Bai et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Hyperoside Attenuates Bleomycin-Induced Pulmonary Fibrosis Development in Mice

et al. 2020

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Idiopathic pulmonary fibrosis (IPF) is a progressive, lethal, and chronic lung disease. There are no effective drug therapies for IPF. Hyperoside, a flavonoid glycoside, has been proven to have anti-inflammatory, anti-fibrosis, antioxidant, and anti-cancer effects. The aim of this study was to explore the role of hyperoside in bleomycin-induced pulmonary fibrosis development in mice. We established the pulmonary fibrosis model by a single intratracheal aerosol injection of bleomycin. Seven days after the bleomycin treatment, the mice were intraperitoneally administered with hyperoside for 14 days. We found that hyperoside treatment ameliorated fibrotic pathological changes and collagen deposition in the lungs of mice with bleomycin-induced pulmonary fibrosis. Hyperoside treatment also reduced the levels of MDA, TNF-a, and IL-6 and increased the activity of SOD. In addition, hyperoside might inhibit the epithelial-mesenchymal transition (EMT) via the AKT/GSK3b pathway. Based on these findings, hyperoside attenuated pulmonary fibrosis development by inhibiting oxidative stress, inflammation, and EMT in the lung tissues of mice with pulmonary fibrosis. Therefore, hyperoside might be a promising candidate drug for the treatment of pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 99%

Hyperoside Attenuates Bleomycin-Induced Pulmonary Fibrosis Development in Mice

et al. 2020

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“…An increase in apoptosis of follicular cells associated with oxidative stress has been observed in idiopathic pulmonary fibrosis (IPF). TGF-β1 contributes to the development of fibrosis and the production of ROS [ 51 , 52 ]. Moreover, tyrosine kinases signaling mediated by fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF) is also crucial in pulmonary fibrosis development.…”

Section: Covid-19 and Pulmonary Fibrosismentioning

confidence: 99%

COVID-19: The Potential Treatment of Pulmonary Fibrosis Associated with SARS-CoV-2 Infection

Lechowicz

Drożdżal

Machaj

et al. 2020

JCM

142

133

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In December 2019, a novel coronavirus, SARS-CoV-2, appeared, causing a wide range of symptoms, mainly respiratory infection. In March 2020, the World Health Organization (WHO) declared Coronavirus Disease 2019 (COVID-19) a pandemic, therefore the efforts of scientists around the world are focused on finding the right treatment and vaccine for the novel disease. COVID-19 has spread rapidly over several months, affecting patients across all age groups and geographic areas. The disease has a diverse course; patients may range from asymptomatic to those with respiratory failure, complicated by acute respiratory distress syndrome (ARDS). One possible complication of pulmonary involvement in COVID-19 is pulmonary fibrosis, which leads to chronic breathing difficulties, long-term disability and affects patients’ quality of life. There are no specific mechanisms that lead to this phenomenon in COVID-19, but some information arises from previous severe acute respiratory syndrome (SARS) or Middle East respiratory syndrome (MERS) epidemics. The aim of this narrative review is to present the possible causes and pathophysiology of pulmonary fibrosis associated with COVID-19 based on the mechanisms of the immune response, to suggest possible ways of prevention and treatment.

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“…Although the role of mitochondrial mtROS in IPF onset and progression is not fully understood approaches to beneficially modulate mtROS levels with antioxidants are currently under investigation (Fig. 4) [164,165].…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 99%

Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis

Phan

Paliogiannis

Nasrallah

et al. 2020

Cell. Mol. Life Sci.

185

108

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Idiopathic pulmonary fibrosis (IPF), the most common form of idiopathic interstitial pneumonia, is a progressive, irreversible, and typically lethal disease characterized by an abnormal fibrotic response involving vast areas of the lungs. Given the poor knowledge of the mechanisms underpinning IPF onset and progression, a better understanding of the cellular processes and molecular pathways involved is essential for the development of effective therapies, currently lacking. Besides a number of established IPF-associated risk factors, such as cigarette smoking, environmental factors, comorbidities, and viral infections, several other processes have been linked with this devastating disease. Apoptosis, senescence, epithelial-mesenchymal transition, endothelial-mesenchymal transition, and epithelial cell migration have been shown to play a key role in IPF-associated tissue remodeling. Moreover, molecules, such as chemokines, cytokines, growth factors, adenosine, glycosaminoglycans, non-coding RNAs, and cellular processes including oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, hypoxia, and alternative polyadenylation have been linked with IPF development. Importantly, strategies targeting these processes have been investigated to modulate abnormal cellular phenotypes and maintain tissue homeostasis in the lung. This review provides an update regarding the emerging cellular and molecular mechanisms involved in the onset and progression of IPF.

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Oxidative Stress in Pulmonary Fibrosis

Cited by 133 publications

References 617 publications

Hyperoside Attenuates Bleomycin-Induced Pulmonary Fibrosis Development in Mice

Hyperoside Attenuates Bleomycin-Induced Pulmonary Fibrosis Development in Mice

COVID-19: The Potential Treatment of Pulmonary Fibrosis Associated with SARS-CoV-2 Infection

Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis

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