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Type: Journal article
Title: Nitrosative stress as a modulator of inflammatory change in a model of Takotsubo syndrome
Author: Surikow, S.Y.
Nguyen, T.H.
Stafford, I.
Chapman, M.
Chacko, S.
Singh, K.
Licari, G.
Raman, B.
Kelly, D.J.
Zhang, Y.
Waddingham, M.T.
Ngo, D.T.
Bate, A.P.
Chua, S.J.
Frenneaux, M.P.
Horowitz, J.D.
Citation: JACC: Basic to Translational Science, 2018; 3(2):213-226
Publisher: Elsevier
Issue Date: 2018
ISSN: 2452-302X
Statement of
Sven Y. Surikow, Thanh H. Nguyen, Irene Stafford, Matthew Chapman, Sujith Chacko, Kuljit Singh, Giovanni Licari, Betty Raman, Darren J. Kelly, Yuan Zhang, Mark T. Waddingham, Doan T. Ngo, Alexander P. Bate, Su Jen Chua, Michael P. Frenneaux, John D. Horowitz
Abstract: 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 β-adrenoceptor signaling (coupled with nitric oxide synthase activation) to elucidate mechanisms of impaired cardiac function in TS and point to potential methods of treatment.
Keywords: Myocardial inflammation; oxidative stress; poly(ADP-ribose) polymerase-1; Takotsubo cardiomyopathy
Rights: ©2018 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license (
DOI: 10.1016/j.jacbts.2017.10.002
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