Oxidative Stress in COPD

Magallón, María; Navarro-García, María Mercedes; Dası́, Francisco

doi:10.3390/jcm8111953

Cited by 11 publications

(6 citation statements)

References 13 publications

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“…Recently, increasing studies have documented oxidative stress to be a major driving mechanism in the pathogenesis of COPD ( Magallón et al, 2019 ). In this study, we first measured the levels of GSH, GSSG and MDA in the serum of patients with COPD and healthy controls, which were important biomarkers of the oxidative and antioxidant balance system.…”

Section: Discussionmentioning

confidence: 99%

LncRNA Nqo1-AS1 Attenuates Cigarette Smoke-Induced Oxidative Stress by Upregulating its Natural Antisense Transcript Nqo1

et al. 2021

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Evidence of the involvement of long noncoding RNAs (lncRNAs) in the pathogenesis of chronic obstructive pulmonary disease (COPD) is growing but still largely unknown. This study aims to explore the expression, functions and molecular mechanisms of Fantom3_F830212L20, a lncRNA that transcribes in an antisense orientation to Nqo1.We name this lncRNA as Nqo1 antisense transcript 1 (Nqo1-AS1). The distribution, expression level and protein coding potential of Nqo1-AS1 were determined. The effects of Nqo1-AS1 on cigarette smoke (CS)-induced oxidative stress were also evaluated. The results showed that Nqo1-AS1 were mainly located in the cytoplasm of mouse alveolar epithelium and had a very low protein coding potential. Nqo1-AS1 (or its human homologue) was increased with the increase of CS exposure. Nqo1-AS1 overexpression enhanced the mRNA and protein levels of Nqo1 and Serpina1 mRNA expression, and attenuated CS-induced oxidative stress, whereas knockdown of Nqo1-AS1 significantly decreased Nqo1 and Serpina1 mRNA expressions, and aggravated CS-induced oxidative stress. Nqo1-AS1 increased Nqo1 mRNA stability and upregulated Nqo1 expression through antisense pairing with Nqo1 3′UTR. In conclusion, these results suggest that Nqo1-AS1 attenuates CS-induced oxidative stress by increasing Nqo1 mRNA stability and upregulating Nqo1 expression, which might serve as a novel approach for the treatment of COPD.

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Section: Discussionmentioning

confidence: 99%

LncRNA Nqo1-AS1 Attenuates Cigarette Smoke-Induced Oxidative Stress by Upregulating its Natural Antisense Transcript Nqo1

et al. 2021

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“…When the defence mechanisms cannot prevent ROS accumulation, the activation of specific signalling pathways causes changes in gene expression and protein synthesis. All these effects led to the hypothesis that increased free radicals and oxidative damage cause an increase in cell damage, which leads to the development of various pathological conditions, such as carcinogenesis [ 13 ], chronic inflammation [ 14 ], ageing [ 15 ], autoimmunity [ 16 ], cardiovascular diseases [ 17 ], neurodegenerative diseases [ 18 ], and respiratory diseases [ 3 ], among others.…”

Section: What Is Oxidative Stress?mentioning

confidence: 99%

“…One of their functions is to activate inflammatory intracellular signalling pathways, leading to the immune system activation [ 2 ]. However, when ROS appear in excess and accumulate within the cells, they create a highly oxidative state that can cause severe and irreparable damage to the tissues either directly or through altering signaling pathways [ 3 ]. Endoplasmic reticulum (ER) stress is the consequence of the accumulation of misfolded proteins in the ER lumen.…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases

Magallón

Carrión

Bañuls

et al. 2021

JCM

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Several studies have shown that some rare respiratory diseases, such as alpha-1 antitrypsin deficiency (AATD), idiopathic pulmonary fibrosis (IPF), cystic fibrosis (CF), and primary ciliary dyskinesia (PCD) present oxidative stress (OS) and endoplasmic reticulum (ER) stress. Their involvement in these pathologies and the use of antioxidants as therapeutic agents to minimize the effects of OS are discussed in this review.

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“…Due to long-term smoking of COPD patients, the CO contained in the smoke significantly reduces the oxygen-binding capacity of hemoglobin, in keeping with previous reports. 30 In light of results demonstrating that oxidative stress and chronic inflammatory response damage the lung parenchyma, and result in respiratory and motor muscles' atrophy to different degrees, further reducing oxygen uptake capacity, 31,32 we hypothesized that this is one of the reasons leading to the non-mitochondrial production of metabolic energy by the anaerobic pathway.…”

Section: Mechanism Of Energy Metabolism and Overall Comparison Of Metabolitesmentioning

confidence: 99%

Metabolomic profiling of anaerobic and aerobic energy metabolic pathways in chronic obstructive pulmonary disease

Xue

Zeng

Lin

et al. 2021

Exp Biol Med (Maywood)

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While there is no cure for chronic obstructive pulmonary disease (COPD), its progressive nature and the formidable challenge to manage its symptoms warrant a more extensive study of the pathogenesis and related mechanisms. A new emphasis on COPD study is the change of energy metabolism. For the first time, this study investigated the anaerobic and aerobic energy metabolic pathways in COPD using the metabolomic approach. Metabolomic analysis was used to investigate energy metabolites in 140 COPD patients. The significance of energy metabolism in COPD was comprehensively explored by the Global Initiative for Chronic Obstructive Lung Disease–GOLD grading, acute exacerbation vs. stable phase (either clinical stability or four-week stable phase), age group, smoking index, lung function, and COPD Assessment Test (CAT) score. Through comprehensive evaluation, we found that COPD patients have a significant imbalance in the aerobic and anaerobic energy metabolisms in resting state, and a high tendency of anaerobic energy supply mechanism that correlates positively with disease progression. This study highlighted the significance of anaerobic and low-efficiency energy supply pathways in lung injury and linked it to the energy-inflammation-lung ventilatory function and the motion limitation mechanism in COPD patients, which implies a novel therapeutic direction for this devastating disease.

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Oxidative Stress in COPD

Cited by 11 publications

References 13 publications

LncRNA Nqo1-AS1 Attenuates Cigarette Smoke-Induced Oxidative Stress by Upregulating its Natural Antisense Transcript Nqo1

LncRNA Nqo1-AS1 Attenuates Cigarette Smoke-Induced Oxidative Stress by Upregulating its Natural Antisense Transcript Nqo1

Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases

Metabolomic profiling of anaerobic and aerobic energy metabolic pathways in chronic obstructive pulmonary disease

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