A Mechanism for Statin-Induced Susceptibility to Myopathy.
Ca2+, calcium
FDB, flexor digitorum brevis
FKBP12, FK506 binding protein (calstabin)
GAS, gastrocnemius
HADHA, hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase
HMG CoA, 3-hydroxy-3-methylglutaryl coenzyme A
L-NAME, N(ω)-nitro-L-arginine methyl ester
NOS, nitric oxide synthase
PGC1α, peroxisome proliferator-activated receptor γ co-activator 1α
RNS, reactive nitrogen species
ROS, reactive oxygen species
RyR, ryanodine receptor
SOD, superoxide dismutase
SR, sarcoplasmic reticulum
TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling
calcium leak
exercise
myopathy
ryanodine receptor
statin
Journal
JACC. Basic to translational science
ISSN: 2452-302X
Titre abrégé: JACC Basic Transl Sci
Pays: United States
ID NLM: 101677259
Informations de publication
Date de publication:
Aug 2019
Aug 2019
Historique:
received:
24
01
2019
revised:
27
03
2019
accepted:
27
03
2019
entrez:
31
8
2019
pubmed:
31
8
2019
medline:
31
8
2019
Statut:
epublish
Résumé
This study aimed to identify a mechanism for statin-induced myopathy that explains its prevalence and selectivity for skeletal muscle, and to understand its interaction with moderate exercise. Statin-associated adverse muscle symptoms reduce adherence to statin therapy; this limits the effectiveness of statins in reducing cardiovascular risk. The issue is further compounded by perceived interactions between statin treatment and exercise. This study examined muscles from individuals taking statins and rats treated with statins for 4 weeks. In skeletal muscle, statin treatment caused dissociation of the stabilizing protein FK506 binding protein (FKBP12) from the sarcoplasmic reticulum (SR) calcium (Ca
Identifiants
pubmed: 31468006
doi: 10.1016/j.jacbts.2019.03.012
pii: S2452-302X(19)30131-7
pmc: PMC6712048
doi:
Types de publication
Journal Article
Langues
eng
Pagination
509-523Subventions
Organisme : British Heart Foundation
ID : RG/16/6/32233
Pays : United Kingdom
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