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

J Cell Physiol. 2020 Feb;235(2):1438-1452. doi: 10.1002/jcp.29064. Epub 2019 Jul 11.


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.

Keywords: SIRT1; STEMI; hyperglycemia; miR33; oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Cohort Studies
  • Coronary Thrombosis / metabolism
  • Coronary Thrombosis / pathology*
  • Endothelial Cells / metabolism
  • Gene Silencing
  • Humans
  • Hyperglycemia / metabolism
  • Hyperglycemia / pathology*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Myocardial Infarction / metabolism
  • Myocardial Infarction / pathology*
  • Sirtuin 1 / genetics
  • Sirtuin 1 / metabolism*


  • MIRN33a microRNA, human
  • MicroRNAs
  • SIRT1 protein, human
  • Sirtuin 1