The Rise of Mitochondria in Peripheral Arterial Disease Physiopathology: Experimental and Clinical Data.
antioxidant
apoptosis
calcium retention capacity
ischemia-reperfusion
mitochondria
oxidative stress
peripheral arterial disease
reactive oxygen species
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
02 Dec 2019
02 Dec 2019
Historique:
received:
10
11
2019
revised:
27
11
2019
accepted:
29
11
2019
entrez:
8
12
2019
pubmed:
8
12
2019
medline:
8
12
2019
Statut:
epublish
Résumé
Peripheral arterial disease (PAD) is a frequent and serious condition, potentially life-threatening and leading to lower-limb amputation. Its pathophysiology is generally related to ischemia-reperfusion cycles, secondary to reduction or interruption of the arterial blood flow followed by reperfusion episodes that are necessary but also-per se-deleterious. Skeletal muscles alterations significantly participate in PAD injuries, and interestingly, muscle mitochondrial dysfunctions have been demonstrated to be key events and to have a prognosis value. Decreased oxidative capacity due to mitochondrial respiratory chain impairment is associated with increased release of reactive oxygen species and reduction of calcium retention capacity leading thus to enhanced apoptosis. Therefore, targeting mitochondria might be a promising therapeutic approach in PAD.
Identifiants
pubmed: 31810355
pii: jcm8122125
doi: 10.3390/jcm8122125
pmc: PMC6947197
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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