Imbalance between endothelial damage and repair capacity in chronic obstructive pulmonary disease

García-Lucio, Jéssica; Peinado, Víctor I.; Jover, Lluís; Pozo, Roberto Del; Blanco, Isabel; Bonjoch, Cristina; Coll-Bonfill, Núria; Paul, Tanja; Tura-Ceide, Olga; Barberà, Joan Albert

doi:10.1371/journal.pone.0195724

Cited by 29 publications

(50 citation statements)

References 46 publications

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“…Results of the present study indicate that pulmonary and systemic vascular impairments are interrelated in COPD. These findings concur with the previous observations of altered markers of vascular competence (defined as an imbalance between injury and repair capacity of the endothelium) in COPD patients with PVD, 5 suggesting common pathways in the pathobiology of alterations in both vascular territories.…”

Section: Discussionsupporting

confidence: 92%

“… 1 Indeed, cardiovascular disease is a major cause of death in COPD patients, accounting for 25% of the overall mortality. 2 Previous studies have shown that COPD is associated with changes in systemic vascular function 3 , 4 and circulating biomarkers of vascular competence 5 thereby suggesting the presence of associated peripheral artery disease. 6 The severity of endothelial dysfunction in systemic arteries, as assessed by flow-mediated dilation (FMD), 7 correlates with the severity of airflow obstruction and the extent of emphysema in COPD.…”

Section: Introductionmentioning

confidence: 99%

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<p>Association Between Systemic and Pulmonary Vascular Dysfunction in COPD</p>

Piccari¹,

Pozo²,

Blanco³

et al. 2020

COPD

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Introduction: In chronic obstructive pulmonary disease (COPD), endothelial dysfunction and stiffness of systemic arteries may contribute to increased cardiovascular risk. Pulmonary vascular disease (PVD) is frequent in COPD. The association between PVD and systemic vascular dysfunction has not been thoroughly evaluated in COPD. Methods: A total of 108 subjects were allocated into four groups (non-smoking controls, smoking controls, COPD without PVD and COPD with PVD). In systemic arteries, endothelial dysfunction was assessed by flow-mediated dilation (FMD) and arterial stiffness by pulse wave analysis (PWA) and pulse wave velocity (PWV). PVD was defined by a mean pulmonary artery pressure (PAP) ≥25 mmHg at right heart catheterization or by a tricuspid regurgitation velocity >2.8 m/s at doppler echocardiography. Biomarkers of inflammation and endothelial damage were assessed in peripheral blood. Results: FMD was lower in COPD patients, with or without PVD, compared to nonsmoking controls; and in patients with COPD and PVD compared to smoking controls. PWV was higher in COPD with PVD patients compared to both non-smoking and smoking controls in a model adjusted by age and the Framingham score; PWV was also higher in patients with COPD and PVD compared to COPD without PVD patients in the non-adjusted analysis. FMD and PWV correlated significantly with forced expiratory volume in the first second (FEV 1), diffusing capacity for carbon monoxide (DL CO) and systolic PAP. FMD and PWV were correlated in all subjects. Discussion: We conclude that endothelial dysfunction of systemic arteries is common in COPD, irrespective if they have PVD or not. COPD patients with PVD show increased stiffness and greater impairment of endothelial function in systemic arteries. These findings suggest the association of vascular impairment in both pulmonary and systemic territories in a subset of COPD patients.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

<p>Association Between Systemic and Pulmonary Vascular Dysfunction in COPD</p>

Piccari¹,

Pozo²,

Blanco³

et al. 2020

COPD

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“…For the request "endothelium + COPD," it offers 335 publications, of which 72 after 2015, and for the request "endothelium + smoking," it offers 1859 publications, of which 188 after 2015. This indicates the relevance of this area of research and demonstrates the hopes of researchers finding new opportunities for therapeutic and prophylactic effects on this relationship in the pathogenesis of tobacco-related lesions, COPD, and emphysema [17][18][19][20][21][22][23].…”

Section: Endothelium-related and Neuro-mediated Mechanisms Of Emphysementioning

confidence: 69%

Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms

Невзорова¹,

Brodskaya²,

Гилифанов³

2020

Update in Respiratory Diseases

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This chapter describes endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease (COPD) and smoking on the basis of previously completed studies, literature data, and own researches. As components of neurogenic inflammation in the processes of tissue remodeling in emphysema, we describe the distribution and activity of the substance P, neurokinin-1 and its receptor, tissue metalloproteinases and their tissue inhibitors in the lungs during the entire experimental period, the modeling of COPD in rats with a smoking model. We also analyzed the content of neurokinin system markers, the localization, and markers of tissue metalloproteinases in human lung tissue structures. We have confidence that there is a special morphofunctional continuum of development of lower respiratory tract remodeling in response to chronic exposure to tobacco smoke and the development of inflammation in COPD. New data suggest that imbalance of neuro-mediated interactions, alteration of vasomotoric signaling mechanisms, secretion, mucociliary clearance, cytoprotection involving substance P-dependent components with impaired content, and development of dystopia of matrix metalloproteinases and their tissue inhibitors are involved in the initiation of morphological restructuring. Research in this direction should be continued to allow approaches to the development of preventive and therapeutic strategies for emphysema.

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“…It has been shown that COPD patients present endothelial dysfunction in both pulmonary and systemic arteries at early disease stages [7–9]. This endothelial damage may result from an imbalance between vascular injury and the body’s repair capacity [10].…”

Section: Introductionmentioning

confidence: 99%

“…Reduced number and function of circulating PCs has been established as an independent prognostic factor associated with endothelial dysfunction, high cardiovascular risk and increased mortality [14–16]. In COPD, few studies to date have investigated the number of circulating PCs [10, 12, 17]. We and others have previously shown reduced levels of circulating PCs in COPD patients, as compared to controls [10, 12, 17].…”

Section: Introductionmentioning

confidence: 99%

Progenitor cell mobilisation and recruitment in pulmonary arteries in chronic obstructive pulmonary disease

et al. 2019

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Background Pulmonary vascular abnormalities are a characteristic feature of chronic obstructive pulmonary disease (COPD). Cigarette smoking is the most important risk factor for COPD. It is believed that its constant exposure triggers endothelial cell damage and vascular remodelling. Under pathological conditions, progenitor cells (PCs) are mobilized from the bone marrow and recruited to sites of vascular injury. The aim of the study was to investigate whether in COPD the number of circulating PCs is related to the presence of bone marrow-derived cells in pulmonary arteries and the association of these phenomena to both systemic and pulmonary endothelial dysfunction. Methods Thirty-nine subjects, 25 with COPD, undergoing pulmonary resection because of a localized carcinoma, were included. The number of circulating PCs was assessed by flow cytometry using a triple combination of antibodies against CD45, CD133 and CD34. Infiltrating CD45 + cells were identified by immunohistochemistry in pulmonary arteries. Endothelial function in systemic and pulmonary arteries was measured by flow-mediated dilation and adenosine diphosphate-induced vasodilation, respectively. Results COPD patients had reduced numbers of circulating PCs ( p < 0.05) and increased numbers of CD45 + cells (< 0.05) in the pulmonary arterial wall than non-COPD subjects, being both findings inversely correlated (r = − 0.35, p < 0.05). In pulmonary arteries, the number of CD45 + cells correlated with the severity of vascular remodelling (r = 0.4, p = 0.01) and the endothelium-dependent vasodilation (r = − 0.3, p = 0.05). Systemic endothelial function was unrelated to the number of circulating PCs and changes in pulmonary vessels. Conclusion In COPD, the decrease of circulating PCs is associated with their recruitment in pulmonary arteries, which in turn is associated with endothelial dysfunction and vessel remodelling, suggesting a mechanistic link between these phenomena. Our findings are consistent with the notion of an imbalance between endothelial damage and repair capacity in the pathogenesis of pulmonary vascular abnormalities in COPD. Electronic supplementary material The online version of this article (10.1186/s12931-019-1024-z) contains supplementary material, which is available to authorized users.

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Imbalance between endothelial damage and repair capacity in chronic obstructive pulmonary disease

Cited by 29 publications

References 46 publications

<p>Association Between Systemic and Pulmonary Vascular Dysfunction in COPD</p>

<p>Association Between Systemic and Pulmonary Vascular Dysfunction in COPD</p>

Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms

Progenitor cell mobilisation and recruitment in pulmonary arteries in chronic obstructive pulmonary disease

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