New frontiers in the treatment of comorbid cardiovascular disease in chronic obstructive pulmonary disease.
Animals
Anti-Inflammatory Agents
/ therapeutic use
Antioxidants
/ therapeutic use
Cardiovascular Diseases
/ drug therapy
Cardiovascular System
/ drug effects
Comorbidity
Disease Progression
Humans
Inflammation Mediators
/ metabolism
Lung
/ drug effects
Oxidative Stress
/ drug effects
Pulmonary Disease, Chronic Obstructive
/ drug therapy
Risk Factors
Signal Transduction
Treatment Outcome
cardiovascular disease
chronic obstructive pulmonary disease
cigarette smoke
lung inflammation
oxidative stress
vascular dysfunction
Journal
Clinical science (London, England : 1979)
ISSN: 1470-8736
Titre abrégé: Clin Sci (Lond)
Pays: England
ID NLM: 7905731
Informations de publication
Date de publication:
15 04 2019
15 04 2019
Historique:
received:
13
11
2018
revised:
26
03
2019
accepted:
01
04
2019
entrez:
14
4
2019
pubmed:
14
4
2019
medline:
30
1
2020
Statut:
epublish
Résumé
Chronic obstructive pulmonary disease (COPD) is a disease characterised by persistent airflow limitation that is not fully reversible and is currently the fourth leading cause of death globally. It is now well established that cardiovascular-related comorbidities contribute to morbidity and mortality in COPD, with approximately 50% of deaths in COPD patients attributed to a cardiovascular event (e.g. myocardial infarction). Cardiovascular disease (CVD) and COPD share various risk factors including hypertension, sedentarism, smoking and poor diet but the underlying mechanisms have not been fully established. However, there is emerging and compelling experimental and clinical evidence to show that increased oxidative stress causes pulmonary inflammation and that the spill over of pro-inflammatory mediators from the lungs into the systemic circulation drives a persistent systemic inflammatory response that alters blood vessel structure, through vascular remodelling and arterial stiffness resulting in atherosclerosis. In addition, regulation of endothelial-derived vasoactive substances (e.g. nitric oxide (NO)), which control blood vessel tone are altered by oxidative damage of vascular endothelial cells, thus promoting vascular dysfunction, a key driver of CVD. In this review, the detrimental role of oxidative stress in COPD and comorbid CVD are discussed and we propose that targeting oxidant-dependent mechanisms represents a novel strategy in the treatment of COPD-associated CVD.
Identifiants
pubmed: 30979844
pii: CS20180316
doi: 10.1042/CS20180316
pmc: PMC6465303
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Antioxidants
0
Inflammation Mediators
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
885-904Informations de copyright
© 2019 The Author(s).
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