Assessment of endothelial dysfunction in idiopathic pulmonary fibrosis

Elshazly, Mostafa; Hosny, Hossam; Abdel-Hafiz, H.; Zakaria, Ayman; El-kaffas, Khaled Helmy; Okasha, Nireen

doi:10.1016/j.ejcdt.2013.08.016

Cited by 6 publications

(7 citation statements)

References 21 publications

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“…The authors hypothesized, that recurrent lectin-mediated vascular injuries might induce an endothelial dysfunction, leading to pulmonary inflammation and fibrosis. In line, the presence of a vasculopathy in IPF patients has been confirmed by observational studies (30,31). However, it remains unclear to what extent injured endothelial cells contribute to fibrotic processes in IPF, as current models of IPF consider rather disturbed epithelial-mesenchymal interactions as crucial (32).…”

Section: Discussionmentioning

confidence: 89%

Local and Systemic Concentrations of Pattern Recognition Receptors of the Lectin Pathway of Complement in a Cohort of Patients With Interstitial Lung Diseases

et al. 2020

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Complement in Interstitial Lung Diseases p = 0.44; BALF, 37.5 vs. 24.6 ng/ml, p = 0.7) as well as lower ficolin-2 plasma levels (plasma 1111 vs. 1647 ng/ml, p = 0.11). Ficolin-2 plasma levels were inversely correlated with the forced vital capacity (r = 0.55, p = 0.1). Conclusion: This is the first study to simultaneously assess systemic and local lectin pathway protein levels in ILD patients. Our data suggest an involvement of PRR of the lectin pathway in the pathogenesis of sarcoidosis given the significantly higher BALF levels compared to a control group. Additional analyses in a larger patient cohort are required to confirm or refute a potential effect of local and/or systemic ficolin-2 levels in IPF patients.

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Section: Discussionmentioning

confidence: 89%

Local and Systemic Concentrations of Pattern Recognition Receptors of the Lectin Pathway of Complement in a Cohort of Patients With Interstitial Lung Diseases

et al. 2020

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“… 74 Endothelial dysfunction is a prevalent affection among patients with IPF, representing a possible link between IPF and cardiovascular diseases. 75 This seems to be related to a significantly reduced tissular and circulatory expression of the vascular endothelium growth factor (VEGF) in patients with IPF. 76 Also, in smokers and patients with pulmonary fibrosis, there is a decreased VEGF level in the broncho-alveolary lavage (BAL), meaning that it (at least) accompanies the lung lesions among these patients.…”

Section: Discussionmentioning

confidence: 99%

“…Endothelial involvement seems to be linked to preexisting cardiovascular diseases and diabetes mellitus and is more related to vasoconstriction after the attenuation of agonist-mediated endothelial vasodilation . Endothelial dysfunction is a prevalent affection among patients with IPF, representing a possible link between IPF and cardiovascular diseases . This seems to be related to a significantly reduced tissular and circulatory expression of the vascular endothelium growth factor (VEGF) in patients with IPF .…”

Section: Discussionmentioning

confidence: 99%

“A Chain Only as Strong as Its Weakest Link”: An Up-to-Date Literature Review on the Bidirectional Interaction of Pulmonary Fibrosis and COVID-19

Criṣan-Dabija

Pavel²,

Popa³

et al. 2020

J. Proteome Res.

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The COVID-19 pandemic rapidly became a worldwide healthcare emergency affecting millions of people, with poor outcomes for patients with chronic conditions and enormous pressure on healthcare systems. Pulmonary fibrosis (PF) has been cited as a risk factor for a more severe evolution of COVID-19, primarily because its acute exacerbations are already associated with high mortality. We reviewed the available literature on biochemical, pathophysiological, and pharmacological mechanisms of PF and COVID-19 in an attempt to foresee the particular risk of infection and possible evolution of PF patients if infected with SARS-COV-2. We also analyzed the possible role of medication and risk factors (such as smoking) in the disease’s evolution and clinical course. We found out that there is a complexity of interactions between coexisting idiopathic pulmonary fibrosis/interstitial lung disease (ILD) and COVID-19 disease. Also, patients recovering from severe COVID-19 disease are at serious risk of developing PF. Smokers seem to have, in theory, a chance for a better outcome if they develop a severe form of COVID-19 but statistically are at much higher risk of dying if they become critically ill.

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“…Giving the reported evidence of induced endothelial dysfunction, pulmonary fibrosis may be also prompted as a substantial problem during COVID-19 infection, to the extent that pulmonary post-mortem findings in fatal cases of COVID-19 revealed the presence of extensive fibrotic features as myofibroblastic proliferation or organizing pneumonia (George et al, 2020). The vascular endothelial dysfunction could stimulate the fibrotic consequences via secreting a peptide, namely endothelin-1 (ET-1) (Elshazly et al, 2013), which could induce the release of transforming growth factor-β1 (TGF-β1), a fibrogenic cytokine mainly implicated in driving the pulmonary fibrosis development (Wermuth et al, 2016).…”

Section: Tgf-β1-induced Pulmonary Fibrosis In Covid-19mentioning

confidence: 99%

New putative insights into Neprilysin (NEP)-dependent pharmacotherapeutic role of Roflumilast in treating COVID-19

Tabaa

2020

Preprint

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Nowadays, COVID-19 represents the most serious inflammatory respiratory disease worldwide. Despite of many proposed therapies, no effective medication has been approved yet. Neutrophils appear to be the key mediator for COVID-19-associated inflammatory immunopathologic, thromboembolic and fibrotic complications. Thus, for any therapeutic agent to be more appropriate, it should greatly block the neutrophilic component of COVID-19. One of the effective therapeutic approaches investigated to reduce neutrophils-associated inflammatory lung diseases with less adverse effects was Roflumilast. Being a highly selective PDE4i, roflumilast acts by enhancing cAMP level, that probably potentiates its anti-inflammatory action via increasing NEP activity. Because activating NEP was previously reported to mitigate several airway inflammatory ailments; this review deeply discusses the proposed NEP-based therapeutic properties of roflumilast, which may be of great importance in curing COVID-19. However, further clinical studies are required to confirm this strategy and to evaluate its in-vivo preventive and therapeutic efficacy against COVID-19.

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Assessment of endothelial dysfunction in idiopathic pulmonary fibrosis

Cited by 6 publications

References 21 publications

Local and Systemic Concentrations of Pattern Recognition Receptors of the Lectin Pathway of Complement in a Cohort of Patients With Interstitial Lung Diseases

Local and Systemic Concentrations of Pattern Recognition Receptors of the Lectin Pathway of Complement in a Cohort of Patients With Interstitial Lung Diseases

“A Chain Only as Strong as Its Weakest Link”: An Up-to-Date Literature Review on the Bidirectional Interaction of Pulmonary Fibrosis and COVID-19

New putative insights into Neprilysin (NEP)-dependent pharmacotherapeutic role of Roflumilast in treating COVID-19

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