Skeletal muscle expression of adipose-specific phospholipase in peripheral artery disease.
Aged
Animals
Case-Control Studies
Disease Models, Animal
Female
Gene Expression Regulation, Enzymologic
Humans
Insulin Resistance
Intermittent Claudication
/ enzymology
Ischemia
/ enzymology
Male
Mice, Inbred C57BL
Middle Aged
Muscle, Skeletal
/ enzymology
Peripheral Arterial Disease
/ enzymology
Phospholipases A2, Calcium-Independent
/ genetics
Tumor Suppressor Proteins
/ genetics
Walking
gene expression
genetics
insulin resistance
intermittent claudication
peripheral artery disease (PAD)
Journal
Vascular medicine (London, England)
ISSN: 1477-0377
Titre abrégé: Vasc Med
Pays: England
ID NLM: 9610930
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
pubmed:
28
8
2020
medline:
5
3
2021
entrez:
28
8
2020
Statut:
ppublish
Résumé
Flow-limiting atherosclerotic lesions of arteries supplying the limbs are a cause of symptoms in patients with peripheral artery disease (PAD). Musculoskeletal metabolic factors also contribute to the pathophysiology of claudication, which is manifest as leg discomfort that impairs walking capacity. Accordingly, we conducted a case-control study to determine whether skeletal muscle metabolic gene expression is altered in PAD. Calf skeletal muscle gene expression of patients with PAD and healthy subjects was analyzed using microarrays. The top-ranking gene differentially expressed between PAD and controls (FDR < 0.001) was
Identifiants
pubmed: 32853041
doi: 10.1177/1358863X20947467
doi:
Substances chimiques
Tumor Suppressor Proteins
0
PLAAT3 protein, human
EC 3.1.1.4
Phospholipases A2, Calcium-Independent
EC 3.1.1.4
Plaat3 protein, mouse
EC 3.1.1.4
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
401-410Subventions
Organisme : NHLBI NIH HHS
ID : K12 HL083786
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK036836
Pays : United States