Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome
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Date
2018-04-01Source Title
JACC: Basic to Translational SciencePublisher
ELSEVIER SCIENCE INCAffiliation
Medicine and RadiologyMetadata
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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), pp.213-226. https://doi.org/10.1016/j.jacbts.2017.10.002.Access Status
Open AccessOpen Access at PMC
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058954Abstract
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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