MicroRNA-33 and SIRT1 influence the coronary thrombus burden in hyperglycemic STEMI patients |
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| Authors: | Nunzia D'Onofrio Celestino Sardu Pasquale Paolisso Fabio Minicucci Felice Gragnano Franca Ferraraccio Iacopo Panarese Lucia Scisciola Ciro Mauro Maria Rosaria Rizzo Gelsomina Mansueto Federica Varavallo Giuseppina Brunitto Rosanna Caserta Virginia Tirino Gianpaolo Papaccio Michelangela Barbieri Giuseppe Paolisso Maria Luisa Balestrieri Raffaele Marfella |
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| Affiliation: | 1. Department of Precision Medicine, University of Campania “Luigi Vanvitelli,”, Naples, Italy;2. Department of Advanced Medical and Surgical Sciences, University of Campania “Luigi Vanvitelli,”, Naples, Italy;3. Department of Cardiology, Hospital Cardarelli, Naples, Italy;4. Department of Translational Medical Sciences, University of Campania “Luigi Vanvitelli,”, Naples, Italy;5. Department of Mental Health and Public Medicine, Section of Statistic, University of Campania “Luigi Vanvitelli,”, Naples, Italy;6. Department of Advanced Biomedical Sciences, Legal Medicine Unit, University of Naples Federico II, Naples, Italy;7. Unit of Pathological Anatomy, Aversa Hospital, Caserta, Italy;8. Department of Experimental Medicine, University of Campania “Luigi Vanvitelli,”, Naples, Italy |
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| Abstract: | Primary percutaneous coronary intervention (PPCI) is a pivotal treatment in ST-segment elevation myocardial infarction (STEMI) patients. However, in hyperglycemic-STEMI patients, the incidence of death is still significant. Here, the involvement of sirtuin 1 (SIRT1) and miR33 on the pro-inflammatory/pro-coagulable state of the coronary thrombus was investigated. Moreover, 1-year outcomes in hyperglycemic STEMI in patients subjected to thrombus aspiration before PPCI were evaluated. Results showed that hyperglycemic thrombi displayed higher size and increased miR33, reactive oxygen species, and pro-inflammatory/pro-coagulable markers. Conversely, the hyperglycemic thrombi showed a lower endothelial SIRT1 expression. Moreover, in vitro experiments on endothelial cells showed a causal effect of SIRT1 modulation on the pro-inflammatory/pro-coagulative state via hyperglycemia-induced miR33 expression. Finally, SIRT1 expression negatively correlated with STEMI outcomes. These observations demonstrate the involvement of the miR33/SIRT1 pathway in the increased pro-inflammatory and pro-coagulable state of coronary thrombi in hyperglycemic STEMI patients. |
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| Keywords: | hyperglycemia miR33 oxidative stress SIRT1 STEMI |
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