Chronic Obstructive Pulmonary Disease and the Cardiovascular System: Vascular Repair and Regeneration as a Therapeutic Target

Karnati, Srikanth; Seimetz, Michael; Kleefeldt, Florian; Sonawane, Avinash; Madhusudhan, Thati; Bachhuka, Akash; Kosanovic, Djuro; Weißmann, Norbert; Krüger, Karsten; Ergün, Süleyman

doi:10.3389/fcvm.2021.649512

Cited by 34 publications

(19 citation statements)

References 297 publications

(273 reference statements)

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“…COPD is often combined with other chronic inflammatory diseases [such as cardiovascular disease ( 76 ) and asthma ( 52 )], which may influence serum resistin levels. In addition, resistin levels were significantly increased in patients with acute exacerbation COPD ( 30 ).…”

Section: Discussionmentioning

confidence: 99%

Resistin as a Systemic Inflammation-Related Biomarker for Sarcopenia in Patients With Chronic Obstructive Pulmonary Disease

Gao

Deng

et al. 2022

Front. Nutr.

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BackgroundSarcopenia is common in patients with chronic obstructive pulmonary disease (COPD) and is mainly caused by systemic inflammation. Resistin acts as a proinflammatory cytokine and is involved in the activation of multiple inflammatory signaling pathways. The aim of this study was to determine the relationship between resistin levels and systemic inflammation and to assess the clinical value of circulating resistin for sarcopenia in patients with COPD.MethodsIn this prospective observational study, we enrolled 235 patients with COPD who were divided into development and validation sets. The definition of sarcopenia followed the guidelines from the Asian Working Group for Sarcopenia. Serum concentrations of resistin and TNF-α were measured using an enzyme-linked immunosorbent assay (ELISA).ResultsIn this study, higher serum resistin levels were significantly associated with lower skeletal muscle mass and muscular strength. The serum resistin levels in patients with sarcopenia were significantly higher than those in patients without sarcopenia. The serum resistin level had positive correlations with the serum TNF-α level (r = 0.250, p = 0.007). The predictive efficacy of the serum resistin level (AUC: 0.828) for sarcopenia was superior to that of the serum TNF-α level (AUC: 0.621). The cutoff point (7.138 ng/ml) for the serum resistin level was validated in the validation set (AUC: 0.818).ConclusionsSerum resistin levels were associated with systemic inflammation and can be used accurately and easily to predict sarcopenia in patients with COPD.

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Section: Discussionmentioning

confidence: 99%

Resistin as a Systemic Inflammation-Related Biomarker for Sarcopenia in Patients With Chronic Obstructive Pulmonary Disease

Gao

Deng

et al. 2022

Front. Nutr.

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“…Pulmonary ECs are an essential component of the gas exchange machinery of the lung alveolus, which can be divided into macrovascular and microvascular endothelial cells [18,19]. These cells are particularly interesting due to their potential for a number of important pathologic consequences upon infection, and during the process of recovery from infections or inflammation [20]. For instance, transdifferentiation of ECs or weakening of the endothelium, can occur.…”

Section: The Pulmonary Endothelial Cellmentioning

confidence: 99%

Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections

Vlahopoulos

Wang

Xue

et al. 2021

Cells

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The bronchial vascular endothelial network plays important roles in pulmonary pathology during respiratory viral infections, including respiratory syncytial virus (RSV), influenza A(H1N1) and importantly SARS-Cov-2. All of these infections can be severe and even lethal in patients with underlying risk factors.A major obstacle in disease prevention is the lack of appropriate efficacious vaccine(s) due to continuous changes in the encoding capacity of the viral genome, exuberant responsiveness of the host immune system and lack of effective antiviral drugs. Current management of these severe respiratory viral infections is limited to supportive clinical care. The primary cause of morbidity and mortality is respiratory failure, partially due to endothelial pulmonary complications, including edema. The latter is induced by the loss of alveolar epithelium integrity and by pathological changes in the endothelial vascular network that regulates blood flow, blood fluidity, exchange of fluids, electrolytes, various macromolecules and responses to signals triggered by oxygenation, and controls trafficking of leukocyte immune cells. This overview outlines the latest understanding of the implications of pulmonary vascular endothelium involvement in respiratory distress syndrome secondary to viral infections. In addition, the roles of infection-induced cytokines, growth factors, and epigenetic reprogramming in endothelial permeability, as well as emerging treatment options to decrease disease burden, are discussed.

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“…COPD is caused by persistent, often progressive airflow limitation in the lungs, and it includes the conditions of chronic bronchitis and emphysema. 2 More than 3 million people die from COPD every year worldwide, 3 and COPD is expected to become the third leading cause of death globally by 2030. 4 Despite the worldwide prevalence of this disease, it remains largely underdiagnosed and undertreated.…”

Section: Introductionmentioning

confidence: 99%

Identification of Dysregulated Mechanisms and Candidate Gene Markers in Chronic Obstructive Pulmonary Disease

Lin¹,

Xue²,

Su³

et al. 2022

COPD

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Purpose This study aimed to identify candidate gene markers that may facilitate chronic obstructive pulmonary disease (COPD) diagnosis and treatment. Methods The GSE47460 and GSE151052 datasets were analyzed to identify differentially expressed mRNAs (DEmRs) between COPD patients and controls. DEmRs that were differentially expressed in the same direction in both datasets were analyzed for functional enrichment and for coexpression. Genes from the largest three modules were tested for their ability to diagnose COPD based on the area under the receiver operating characteristic curve (AUC). Genes with AUC > 0.7 in both datasets were used to perform regression based on the “least absolute shrinkage and selection operator” in order to identify feature genes. We also identified differentially expressed miRNAs (DEmiRs) between COPD patients and controls using the GSE38974 dataset, then constructed a regulatory network. We also examined associations between feature genes and immune cell infiltration in COPD, and we identified methylation markers of COPD using the GSE63704 dataset. Results A total of 1350 genes differentially regulated in the same direction in the GSE47460 and GSE151052 datasets were found. The genes were significantly enriched in immune-related biological functions. Of 186 modules identified using MEGENA, the largest were C1_ 6, C1_ 3, and C1_ 2. Of the 22 candidate genes screened based on AUC, 11 feature genes emerged from analysis of a subset of GSE47460 data, which we validated using another subset of GSE47460 data as well as the independent GSE151052 dataset. Feature genes correlated significantly with infiltration by immune cells. The feature genes GPC4 and RS1 were predicted to be regulated by miR-374a-3p. We identified 117 candidate methylation markers of COPD, including PRRG4. Conclusion The feature genes we identified may be potential diagnostic markers and therapeutic targets in COPD. These findings provide new leads for exploring disease mechanisms and targeted treatments.

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Chronic Obstructive Pulmonary Disease and the Cardiovascular System: Vascular Repair and Regeneration as a Therapeutic Target

Cited by 34 publications

References 297 publications

Resistin as a Systemic Inflammation-Related Biomarker for Sarcopenia in Patients With Chronic Obstructive Pulmonary Disease

Resistin as a Systemic Inflammation-Related Biomarker for Sarcopenia in Patients With Chronic Obstructive Pulmonary Disease

Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections

Identification of Dysregulated Mechanisms and Candidate Gene Markers in Chronic Obstructive Pulmonary Disease

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