Skeletal and Respiratory Muscle Dysfunctions in Pulmonary Arterial Hypertension.
Pulmonary arterial hypertension
catabolism
exercise
mitochondria
oxygen supply
respiratory muscles
skeletal muscles
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
03 Feb 2020
03 Feb 2020
Historique:
received:
15
12
2019
revised:
20
01
2020
accepted:
28
01
2020
entrez:
8
2
2020
pubmed:
8
2
2020
medline:
8
2
2020
Statut:
epublish
Résumé
Pulmonary arterial hypertension (PAH) is a rare disease, which leads to the progressive loss and remodeling of the pulmonary vessels, right heart failure, and death. Different clinical presentations can be responsible for such a bad prognosis disease and the underlying mechanisms still need to be further examined. Importantly, skeletal and respiratory muscle abnormalities largely contribute to the decreased quality of life and exercise intolerance observed in patients with PAH. At the systemic level, impaired oxygen supply through reduced cardiac output and respiratory muscle dysfunctions, which potentially result in hypoxemia, is associated with altered muscles vascularization, inflammation, enhanced catabolic pathways, and impaired oxygen use through mitochondrial dysfunctions that are likely participate in PAH-related myopathy. Sharing new insights into the pathological mechanisms of PAH might help stimulate specific research areas, improving the treatment and quality of life of PAH patients. Indeed, many of these muscular impairments are reversible, strongly supporting the development of effective preventive and/or therapeutic approaches, including mitochondrial protection and exercise training.
Identifiants
pubmed: 32028638
pii: jcm9020410
doi: 10.3390/jcm9020410
pmc: PMC7073630
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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