Metabolomics in COPD

Gea, Joaquim; Enríquez-Rodríguez, César J.; Pascual-Guardia, Sergi

doi:10.1016/j.arbres.2022.12.018

Cited by 8 publications

(2 citation statements)

References 115 publications

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“…Future research should prioritize patient-centric approaches that consider the diverse phenotypes and endotypes within the COPD spectrum [53]. Integrating patient-reported outcomes, quality of life assessments, and real-world data into research frameworks will ensure that interventions are not only scientifically rigorous but also meaningful and impactful for individuals living with COPD.…”

Section: Patient-centric Approachesmentioning

confidence: 99%

Mitochondrial Dysfunction in Chronic Obstructive Pulmonary Disease: Unraveling the Molecular Nexus

Li,

Liu,

Liu

2024

Biomedicines

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Chronic obstructive pulmonary disease (COPD) is a prevalent and debilitating respiratory disorder characterized by persistent airflow limitation and chronic inflammation. In recent years, the role of mitochondrial dysfunction in COPD pathogenesis has emerged as a focal point of investigation. This review endeavors to unravel the molecular nexus between mitochondrial dysfunction and COPD, delving into the intricate interplay of oxidative stress, bioenergetic impairment, mitochondrial genetics, and downstream cellular consequences. Oxidative stress, a consequence of mitochondrial dysfunction, is explored as a driving force behind inflammation, exacerbating the intricate cascade of events leading to COPD progression. Bioenergetic impairment sheds light on the systemic consequences of mitochondrial dysfunction, impacting cellular functions and contributing to the overall energy imbalance observed in COPD patients. This review navigates through the genetic landscape, elucidating the role of mitochondrial DNA mutations, variations, and haplogroups in COPD susceptibility and severity. Cellular consequences, including apoptosis, autophagy, and cellular senescence, are examined, providing insights into the intricate mechanisms by which mitochondrial dysfunction influences COPD pathology. Therapeutic implications, spanning antioxidant strategies, mitochondria-targeted compounds, and lifestyle modifications, are discussed in the context of translational research. Important future directions include identifying novel biomarkers, advancing mitochondria-targeted therapies, and embracing patient-centric approaches to redefine COPD management. This abstract provides a comprehensive overview of our review, offering a roadmap for understanding and addressing the molecular nexus between mitochondrial dysfunction and COPD, with potential implications for precision medicine and improved patient outcomes.

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Section: Patient-centric Approachesmentioning

confidence: 99%

Mitochondrial Dysfunction in Chronic Obstructive Pulmonary Disease: Unraveling the Molecular Nexus

Li,

Liu,

Liu

2024

Biomedicines

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“…Metabolomics is a powerful tool used to analyze the composition and content changes of small molecule metabolites during a specific period of time. It provides insights into the relative relationship between metabolites and physiological and pathological changes [ 7 ]. There are three commonly used detection methods for metabolomics including nuclear magnetic resonance, gas chromatography-mass spectrometry (GC-MS), and liquid chromatograph mass spectrometry (LC-MS) [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Metabolomics and transcriptomics of embryonic livers reveal hypoxia adaptation of Tibetan chickens

Xue,

Yu,

Yang

et al. 2024

BMC Genomics

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Background Exploring the hypoxia adaptation mechanism of Tibetan chicken is of great significance for revealing the survival law of Tibetan chicken and plateau animal husbandry production. To investigate the hypoxia adaptation of Tibetan chickens (TBCs), an integrative metabolomic-transcriptomic analysis of the liver on day 18 of embryonic development was performed. Dwarf laying chickens (DLCs), a lowland breed, were used as a control. Results A total of 1,908 metabolites were identified in both TBCs and DLCs. Energy metabolism and amino acid metabolism related differentially regulated metabolites (DRMs) were significantly enriched under hypoxia. Important metabolic pathways including the TCA cycle and arginine and proline metabolism were screened; PCK1, SUCLA2, and CPS1 were found to be altered under hypoxic conditions. In addition, integrated analysis suggested potential differences in mitochondrial function, which may play a crucial role in the study of chicken oxygen adaptation. Conclusions These results suggest that hypoxia changed the gene expression and metabolic patterns of embryonic liver of TBCs compared to DLCs. Our study provides a basis for uncovering the molecular regulation mechanisms of hypoxia adaptation in TBCs with the potential application of hypoxia adaptation research for other animals living on the Qinghai-Tibet plateau, and may even contribute to the study of diseases caused by hypoxia.

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Fatty Acid Oxidation‐Glycolysis Metabolic Transition Affects ECM Homeostasis in Silica‐Induced Pulmonary Fibrosis

Sun,

Zhou,

Peng

et al. 2024

Advanced Science

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Silicosis is a fatal occupational pulmonary disease that is characterized by irreversible replacement of lung parenchyma by aberrant Exracellular matrix (ECM). Metabolic reprogramming is a crucial mechanism for fibrosis. However, how the metabolic rewiring shifts the ECM homeostasis toward overaccumulation remains unclear. Herein, a phenotype with reduction in fatty acid oxidation (FAO) but enhanced glycolysis in myofibroblasts is shown. Perturbation of the glycolytic and FAO pathways, respectively, reveals distinct roles in the metabolic distribution of ECM deposition and degradation. Suppressed glycolysis leads to a decrease in insoluble ECM, primarily due to the inhibition of ECM‐modifying enzyme activity and a decrease in glycine synthesis. Notably, promoted FAO facilitates the intracellular degradation pathway of ECM. In addition, the findings revealed that hypoxia‐inducible factor‐1 alpha (HIF‐1α) serves as a crucial metabolic regulator in the transition from FAO to glycolysis, thereby playing a significant role in ECM deposition in silica‐induced pulmonary fibrosis. Further, the promotion of FAO, inhibition of glycolysis and HIF‐1α reduce ECM production and promote ECM degradation, ultimately impeding the progression of fibrosis and providing therapeutic relief for established pulmonary fibrosis in vivo. These findings unveil the metabolic rewire underpinning the deposition of ECM in silica‐induced lung fibrosis and identify novel targets for promoting regression of pulmonary fibrosis.

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Metabolomics in COPD

Cited by 8 publications

References 115 publications

Mitochondrial Dysfunction in Chronic Obstructive Pulmonary Disease: Unraveling the Molecular Nexus

Mitochondrial Dysfunction in Chronic Obstructive Pulmonary Disease: Unraveling the Molecular Nexus

Metabolomics and transcriptomics of embryonic livers reveal hypoxia adaptation of Tibetan chickens

Fatty Acid Oxidation‐Glycolysis Metabolic Transition Affects ECM Homeostasis in Silica‐Induced Pulmonary Fibrosis

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