Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome.
JACC Basic Transl Sci
; 3(2): 213-226, 2018 Apr.
Article
in En
| MEDLINE
| ID: mdl-30062207
Previous studies have shown that patients with Takotsubo syndrome (TS) have supranormal nitric oxide signaling, and post-mortem studies of TS heart samples revealed nitrosative stress. Therefore, we first showed in a female rat model that isoproterenol induces TS-like echocardiographic changes, evidence of nitrosative stress, and consequent activation of the energy-depleting enzyme poly(ADP-ribose) polymerase-1. We subsequently showed that pre-treatment with an inhibitor of poly(ADP-ribose) polymerase-1 ameliorated contractile abnormalities. These findings thus add to previous reports of aberrant ß-adrenoceptor signaling (coupled with nitric oxide synthase activation) to elucidate mechanisms of impaired cardiac function in TS and point to potential methods of treatment.
3AB, 3-aminobenzamide; ANOVA, analysis of variance; ISO, isoproterenol; LV, left ventricular; NFκB, nuclear factor kappa B; NO, nitric oxide; NOS, nitric oxide synthase; NT, nitrotyrosine; O2, superoxide; ONOO, peroxynitrite; PAR, poly(ADP-ribose); PARP, poly(ADP-ribose) polymerase; TS, Takotsubo syndrome; TXNIP, thioredoxin-interacting protein; Takotsubo cardiomyopathy; myocardial inflammation; oxidative stress; poly(ADP-ribose) polymerase-1
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Type of study:
Prognostic_studies
Language:
En
Journal:
JACC Basic Transl Sci
Year:
2018
Document type:
Article
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