Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome
AuthorSurikow, SY; Nguyen, TH; Stafford, I; Chapman, M; Chacko, S; Singh, K; Licari, G; Raman, B; Kelly, DJ; Zhang, Y; ...
Source TitleJACC: Basic to Translational Science
PublisherELSEVIER SCIENCE INC
University of Melbourne Author/sKelly, Darren
AffiliationMedicine and Radiology
Document TypeJournal Article
CitationsSurikow, 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), pp.213-226. https://doi.org/10.1016/j.jacbts.2017.10.002.
Access StatusOpen Access
Open Access at PMChttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058954
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.
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