Metabolic reprogramming: A driver of cigarette smoke-induced inflammatory lung diseases

Li, Linhui; Yang, David C.H.; Chen, Ching Hsien

doi:10.1016/j.freeradbiomed.2020.12.438

Cited by 19 publications

(15 citation statements)

References 98 publications

(167 reference statements)

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“…Recent evidence suggests that tobacco smoke could lead to metabolic reprogramming 35 . For example, proteomic studies of lung epithelial cells exposed to cigarette smoke revealed an abnormality in oxidative phosphorylation and altered abundance of various enzymes of the tricarboxylic acid cycle.…”

Section: Discussionmentioning

confidence: 99%

Medwakh smoking induces alteration in salivary proteins and cytokine expression: An exploratory investigation employing salivary proteomics analysis

K.G,

Soares,

Rahman

et al. 2024

Preprint

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The study aims to elucidate salivary proteome alterations in medwakh smokers. Saliva samples from 33 medwakh smokers and 30 non-smokers were subjected to proteomic analysis using UHPLC-ESI-QTOF-MS. Saliva samples were analyzed for the production of 13 cytokines using LEGENDplex™ Human Essential Immune Response Panel. Statistical analysis revealed alterations in the abundance of 74 proteins including key immune mediators and inflammatory markers (Accession: PXD045901). Proteins involved in oxidative stress, cell anchorage, and cell metabolic processes were affected in medwakh smokers. Salivary immune response evaluation further validated proteome findings, revealing significantly higher levels of IL-1β, IL-12p70, IL-23, IFN-γ (Th1 cytokines), IL-6 (Th2 cytokine), and MCP-1 (chemokine) in medwakh smokers. The substantial increase in abundance of involucrin suggests stratified squamous cell differentiation and increased cell lysis in the oral cavity of medwakh smokers akin to chronic obstructive pulmonary diseases (COPD). The protein–metabolite joint pathway analysis further showed significantly enriched differentially expressed proteins and metabolites of glycolysis/gluconeogenesis, pentose phosphate, fructose and mannose, nicotinate and nicotinamide, and glutathione metabolism pathways in medwakh smokers. The findings underscore an urgent need for comprehensive public health interventions among youth, including awareness, cessation programs, and promoting healthier lifestyle choices to safeguard the well-being of individuals and communities worldwide.

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Section: Discussionmentioning

confidence: 99%

Medwakh smoking induces alteration in salivary proteins and cytokine expression: An exploratory investigation employing salivary proteomics analysis

K.G,

Soares,

Rahman

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…At a systemic level, CS exposure has been linked to various metabolic syndromes, such as insulin resistance and abnormal lipoprotein metabolism [81]. At cellular level, CS is known to induce the dysregulation of several metabolic pathways [82]. Thus, CS exposure can not only cause microglia activation but likely keep them locked in an activated state, which can further enhance ALS disease progression.…”

Section: Immunometabolismmentioning

confidence: 99%

Pathophysiological Correlation between Cigarette Smoking and Amyotrophic Lateral Sclerosis

et al. 2021

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Cigarette smoke (CS) has been consistently demonstrated to be an environmental risk factor for amyotrophic lateral sclerosis (ALS), although the molecular pathogenic mechanisms involved are yet to be elucidated. Here, we propose different mechanisms by which CS exposure can cause sporadic ALS pathogenesis. Oxidative stress and neuroinflammation are widely implicated in ALS pathogenesis, with blood–spinal cord barrier disruption also recognised to be involved in the disease process. In addition, immunometabolic, epigenetic and microbiome alterations have been implicated in ALS recently. Identification of the underlying pathophysiological mechanisms that underpin CS-associated ALS will drive future research to be conducted into new targets for treatment.

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“…The dysregulation of the metabolic reprogramming process has been linked to a compromised immune system in patients with asthma [8][9][10]. The process of glycolysis which is the main source of energy in the body has been reported to be enhanced in patients with asthma [10].…”

Section: Introductionmentioning

confidence: 99%

Hexokinase 2 aggravates airway inflammation in experimental asthma by regulating airway epithelial cell death

Tian,

Wang,

Fan

et al. 2024

Preprint

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Background Asthma is a prevalent inflammatory lungs disease which poses a substantial global health and economic burden. Abnormal glucose metabolism in asthmatic patients has recently attracted much attention. As a key enzyme in glycolysis, the participation of Hexokinase 2(HK2) in the disease course of asthma has not been fully understudied. Methods In an asthma mouse model, the expression levels of Hexokinase 2 (HK2) were validated, and a mouse model with HK2 specifically knocked out in airway epithelial cells was created to investigate the role of HK2 in bronchial asthma. In vitro cellular experiments involved the overexpression and knockdown of HK2 to study its role and related mechanisms in airway epithelial cell death and airway inflammation in bronchial asthma. Results HK2 is found to have increased expression in both mouse asthma models, especially showing elevated expression in airway epithelial cells. Mice that specifically lacked HK2 in their airway epithelium were observed to be protected from cell death and inflammation during asthma. Moreover, airway epithelial cells treated with HK2 overexpression exacerbated cell death and elevated the expression of inflammatory interleukins, conversely after silencing HK2 in vitro, cell death and inflammatory interleukins expression were greatly improved. We further surmise that HK2 might be involved in the regulation of airway epithelial cell death and airway inflammation through PPIF and VDAC1. Furthermore, the treatment of mice with HK2 inhibitor, 2-DG, markedly attenuated the inflammatory cell infiltration in the pulmonary tissues. Conclusion HK2 plays a crucial role in the occurrence and progression of bronchial asthma, being involved in airway epithelial cell death and airway inflammation.

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Metabolic reprogramming: A driver of cigarette smoke-induced inflammatory lung diseases

Cited by 19 publications

References 98 publications

Medwakh smoking induces alteration in salivary proteins and cytokine expression: An exploratory investigation employing salivary proteomics analysis

Medwakh smoking induces alteration in salivary proteins and cytokine expression: An exploratory investigation employing salivary proteomics analysis

Pathophysiological Correlation between Cigarette Smoking and Amyotrophic Lateral Sclerosis

Hexokinase 2 aggravates airway inflammation in experimental asthma by regulating airway epithelial cell death

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