MicroRNA-33 and SIRT1 influence the coronary thrombus burden in hyperglycemic STEMI patients

被引:71
作者
D'Onofrio, Nunzia [1 ]
Sardu, Celestino [2 ]
Paolisso, Pasquale [2 ]
Minicucci, Fabio [3 ]
Gragnano, Felice [4 ]
Ferraraccio, Franca [5 ]
Panarese, Iacopo [5 ]
Scisciola, Lucia [2 ]
Mauro, Ciro [3 ]
Rizzo, Maria Rosaria [2 ]
Mansueto, Gelsomina [6 ]
Varavallo, Federica [7 ]
Brunitto, Giuseppina [7 ]
Caserta, Rosanna [7 ]
Tirino, Virginia [8 ]
Papaccio, Gianpaolo [8 ]
Barbieri, Michelangela [2 ]
Paolisso, Giuseppe [2 ]
Balestrieri, Maria Luisa [1 ]
Marfella, Raffaele [2 ]
机构
[1] Univ Campania Luigi Vanvitelli, Dept Precis Med, Naples, Italy
[2] Univ Campania Luigi Vanvitelli, Dept Adv Med & Surg Sci, Piazza Miraglia 2, I-80138 Naples, Italy
[3] Hosp Cardarelli, Dept Cardiol, Naples, Italy
[4] Univ Campania Luigi Vanvitelli, Dept Translat Med Sci, Naples, Italy
[5] Univ Campania Luigi Vanvitelli, Sect Stat, Dept Mental Hlth & Publ Med, Naples, Italy
[6] Univ Naples Federico II, Legal Med Unit, Dept Adv Biomed Sci, Naples, Italy
[7] Aversa Hosp, Unit Pathol Anat, Caserta, Italy
[8] Univ Campania Luigi Vanvitelli, Dept Expt Med, Naples, Italy
关键词
hyperglycemia; miR33; oxidative stress; SIRT1; STEMI; TIGHT GLYCEMIC CONTROL; MYOCARDIAL-INFARCTION; ADMISSION HYPERGLYCEMIA; STRESS HYPERGLYCEMIA; INTERVENTION; DIFFERENTIATION; ASPIRATION; SENESCENCE; EXPRESSION; GUIDELINES;
D O I
10.1002/jcp.29064
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:1438 / 1452
页数:15
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