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Surikow SY, Nguyen TH, Stafford I, et al. Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome. JACC Basic Transl Sci. 2018;3(2):213-226doi: 10.1016/j.jacbts.2017.10.002.
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. (2018). Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome. JACC. Basic to translational science, 3(2), 213-226. https://doi.org/10.1016/j.jacbts.2017.10.002
Surikow, Sven Y, et al. "Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome." JACC. Basic to translational science vol. 3,2 (2018): 213-226. doi: https://doi.org/10.1016/j.jacbts.2017.10.002
Surikow SY, Nguyen TH, Stafford I, Chapman M, Chacko S, Singh K, Licari G, Raman B, Kelly DJ, Zhang Y, Waddingham MT, Ngo DT, Bate AP, Chua SJ, Frenneaux MP, Horowitz JD. Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome. JACC Basic Transl Sci. 2018 Apr 18;3(2):213-226. doi: 10.1016/j.jacbts.2017.10.002. eCollection 2018 Apr. PMID: 30062207; PMCID: PMC6058954.
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JACC Basic Transl Sci. 2018 Apr 18;3(2):213-226. doi: 10.1016/j.jacbts.2017.10.002. eCollection 2018 Apr.

Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome.

JACC. Basic to translational science

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

Affiliations

  1. The Queen Elizabeth Hospital, Department of Cardiology, University of Adelaide, South Australia, Australia.
  2. Basil Hetzel Institute, Adelaide, South Australia, Australia.
  3. Department of Medicine, St. Vincent's Hospital, University of Melbourne, Melbourne, Australia.
  4. University of East Anglia, Norfolk, United Kingdom.

PMID: 30062207 PMCID: PMC6058954 DOI: 10.1016/j.jacbts.2017.10.002

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: 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

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