Hypoxic pulmonary vasoconstriction in COPD-associated pulmonary hypertension: been there, done that?

Bogaard, Harm Jan

doi:10.1183/13993003.01191-2017

Cited by 8 publications

(7 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, several pieces of evidence pointed to vascular damage as an independent process that may be previous to alveolar damage. In this respect, there are patients who develop PH prior to hypoxemia, and endothelial dysfunction with mild COPD [5][6][7]. This has also been demonstrated in the pulmonary vasculature of necropsies from healthy smokers and patients with COPD without hypoxemia and in animal models chronically exposed to tobacco smoke [8][9][10][11].…”

Section: Introductionmentioning

confidence: 79%

Direct Effects of Cigarette Smoke in Pulmonary Arterial Cells alter Vascular Tone through Arterial Remodeling and Kv7.4 Channel Dysregulation

Sevilla-Montero¹,

Labrousse-Arias²,

Fernández-Pérez³

et al. 2019

Preprint

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) is a widespread disease, with no curative therapies nowadays. Exposure to cigarette smoking is considered the chief leading cause of COPD. Current drugs therapies improve patient quality of life, however they do not revert the progression of the disease. Therefore, a deeper study of the cellular and molecular mechanisms that underlie this pathology is required to be able to carry out targeted and effective treatments. Although the effects of cigarette smoke in the progressive deterioration of the airway have been extensively studied in COPD patients, its effects on pulmonary vasculature have been unexplored, due to the classic conception that vascular damage is a consequence of alveolar hypoxia and loss of capillary bed. In this paper, we aimed to study the effects of cigarette smoke extract (CSE) in regulating pulmonary arterial cells phenotypic modulation, in particular the effects in fibroblasts (hPAFib) and smooth muscle cells (hPASMC), and in murine pulmonary arteries. Our results demonstrated that CSE exposure had direct effects on hPAFib and hPASMC, promoting a senescent phenotype that in turn contributed, through the secretion of inflammatory molecules, to increase the proliferative potential of non-exposed cells. CSE also increased total ROS levels in hPAFib and hPASMC, and upregulated NADPH oxidase subunits NOX1 and p22 phox . Most importantly, CSE affected cell contractility and dysregulated the expression and activity of voltage-gated K + channel Kv7.4. This contributed to limit vascular responses impairing vasoconstriction and endotheliumdependent and independent relaxation.

show abstract

Section: Introductionmentioning

confidence: 79%

Direct Effects of Cigarette Smoke in Pulmonary Arterial Cells alter Vascular Tone through Arterial Remodeling and Kv7.4 Channel Dysregulation

Sevilla-Montero¹,

Labrousse-Arias²,

Fernández-Pérez³

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…Pulmonary vascular remodeling is an important sign of COPD progression to pulmonary hypertension (11). The existing scholars believe that the pathogenesis of…”

Section: Discussionmentioning

confidence: 99%

“…This also makes us clear about the important role of inflammatory response in the process of pulmonary vascular remodeling (10). Pulmonary vascular remodeling is an important sign of COPD progression to pulmonary hypertension (11). The existing scholars believe that the pathogenesis of pulmonary hypertension is closely related to inflammation.…”

Section: Discussionmentioning

confidence: 99%

Effect of compound Tinglizi Decoction on non-classical pathway of pyroptosis in rats with chronic obstructive pulmonary disease related pulmonary hypertension

Wang¹,

Liu

et al. 2022

Preprint

View full text Add to dashboard Cite

Objective To observe the effect of compound Tinglizi Decoction on non-classical pathway of cell death in rats with pulmonary hypertension, and to explore its mechanism of action in the treatment of COPD-related pulmonary hypertension. Methods 60 male SD rats were randomly divided into Western group, normal group, model group, high-dose group, medium dose group and low-dose group, with 10 rats per group. We detected the protein expression levels of caspase-11, GSDMD and IL-6 by Western blot, detected serum TNF-α by ELISA, and observed the morphology of lung tissue by hematoxylin and eosin (HE) staining. Results In the expression of caspase11, GSDMD, IL-6 mRNA and protein in lung tissue, the model group was significantly higher than the normal group (P < 0.01), and the high-dose group, middle-dose group, low-dose group and western medicine group were significantly lower than the model group (P < 0.01). The levels of serum TNF-α and serum creatinine in the model group were significantly higher than those in the normal group (P < 0.01); and those in the high-dose group, middle-dose group, low-dose group and western medicine group were significantly lower than those in the model group (P < 0.05). Conclusion The mechanism of compound Tinglizi Decoction in the intervention of COPD-related pulmonary hypertension rats is related to the inhibition of non-classical pathway of cell death.

show abstract

“…Hypoxic pulmonary vasoconstriction occurs in COPD patients (without COVID-19) due to reduced ventilation [51], which predisposes to in-situ thrombus formation; this pathophysiology can be worsened by COVID-19. Hypoxic pulmonary vasoconstriction is associated with increased pulmonary hypertension in COPD due to vascular remodelling [52]; again, this may be further worsened by COVID-19.…”

Section: Worse Covid-19 Clinical Outcomes In Chronic Obstructive Pulm...mentioning

confidence: 99%

Chronic obstructive pulmonary disease and COVID-19: interrelationships

Singh

Mathioudakis

Higham

2021

Current Opinion in Pulmonary Medicine

View full text Add to dashboard Cite

Purpose of reviewChronic obstructive pulmonary disease (COPD) and COVID-19 have many potentially negative interrelationships, which may influence the course of infection and clinical outcomes. The aim of this review is to provide clinicians with an up-to-date perspective of the complex interactions between COPD and COVID-19. Recent findingsWe consider mechanisms that could increase SARS-CoV-2 infection susceptibility in COPD, including increased ACE2 expression, reduced antiviral defence and dysfunctional immunity. We review evidence that COPD is associated with worse clinical outcomes from COVID-19 in analyses that have adjusted for confounding factors, and describe the mechanisms responsible. We discuss the use of inhaled corticosteroids in the context of susceptibility to COVID-19, and consider the impact of COVID-19 on the usual care of COPD patients.

show abstract

Hypoxic pulmonary vasoconstriction in COPD-associated pulmonary hypertension: been there, done that?

Cited by 8 publications

References 22 publications

Direct Effects of Cigarette Smoke in Pulmonary Arterial Cells alter Vascular Tone through Arterial Remodeling and Kv7.4 Channel Dysregulation

Direct Effects of Cigarette Smoke in Pulmonary Arterial Cells alter Vascular Tone through Arterial Remodeling and Kv7.4 Channel Dysregulation

Effect of compound Tinglizi Decoction on non-classical pathway of pyroptosis in rats with chronic obstructive pulmonary disease related pulmonary hypertension

Chronic obstructive pulmonary disease and COVID-19: interrelationships

Contact Info

Product

Resources

About