Age-associated declined function of endothelial progenitor cells and its correlation with plasma IL-18 or IL-23

Yuanting Zhu1,2,3, Guoyi Cai1,3, Luyang Lin1,3

  • 1Division of Emergency Medicine, Department of Emergency Intensive Care Unit, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Insights

Aging impairs endothelial progenitor cell (EPC) function in ST-segment elevation myocardial infarction (STEMI) patients, linked to increased inflammatory cytokines IL-18 and IL-23. This suggests new therapeutic targets for elderly STEMI patients.

Area of Science:

  • Cardiology
  • Gerontology
  • Immunology

Background:

  • ST-segment elevation myocardial infarction (STEMI) disproportionately affects the elderly, who experience reduced endothelial progenitor cell (EPC) capacity.
  • The specific impact of aging on EPC function in STEMI patients remains incompletely understood.

Purpose of the Study:

  • To investigate the influence of aging on EPC function in STEMI patients.
  • To explore the relationship between age, EPC function, inflammatory cytokines (IL-18, IL-23), and clinical risk scores (TIMI, GRACE).

Main Methods:

  • Enrolled younger and older STEMI patients.
  • Assessed Thrombolysis in Myocardial Infarction (TIMI) and Global Registry of Acute Coronary Events (GRACE) scores.
  • Measured EPC migration, proliferation, adhesion, and plasma IL-18/IL-23 concentrations.
  • Analyzed correlations between age, EPC function, cytokines, and clinical scores.

Main Results:

  • Older STEMI patients exhibited higher GRACE/TIMI scores and diminished EPC function compared to younger patients.
  • EPC function was inversely correlated with GRACE/TIMI scores.
  • Plasma IL-18 and IL-23 levels were elevated in older patients, negatively correlating with EPC function and positively with GRACE/TIMI scores.
  • Age correlated positively with IL-18/IL-23 and GRACE/TIMI scores, but negatively with EPC function.

Conclusions:

  • Aging impairs EPC function in STEMI, potentially mediated by inflammatory cytokines like IL-18 and IL-23.
  • This study provides insights into the mechanisms underlying aging in STEMI and identifies potential therapeutic targets.
Abstract