The decrease of endothelial progenitor cells caused by high altitude may lead to coronary heart disease

X-Q Ha1, J Li, C-P Mai

  • 1The 940th Hospital of Joint Logistics Support Force of PLA, Lanzhou, Gansu, China. haxiaoqin20@21cn.com.

Insights

Endothelial progenitor cells (EPCs) are reduced in patients with coronary heart disease (CHD). This decrease, potentially linked to high altitude, may elevate inflammatory cytokines, contributing to CHD development.

Area of Science:

  • Cardiovascular Research
  • Cell Biology
  • Environmental Health

Background:

  • Coronary heart disease (CHD) is a significant global health concern.
  • Endothelial progenitor cells (EPCs) play a crucial role in vascular repair and endothelial function.
  • Factors influencing EPC levels and their association with CHD require further investigation.

Purpose of the Study:

  • To investigate the relationship between the number of EPCs and the presence of CHD.
  • To explore potential environmental influences, such as high altitude, on EPC levels and CHD risk.

Main Methods:

  • A case-control study involving 24 CHD patients and 24 matched healthy controls from Lanzhou and Xianyang cities.
  • Measurement of EPC counts.
  • Assay of serum biomarkers including C-reactive protein (CRP), high-sensitivity CRP (hs-CRP), interleukin-8 (IL-8), vascular endothelial growth factor (VEGF), homocysteine (Hcy), hypoxia-inducible factor-1α (HIF-1α), and stromal cell-derived factor 1 (SDF-1α).

Main Results:

  • EPC numbers were significantly lower in CHD patients compared to controls.
  • Higher levels of total cholesterol (TC), LDL, and CRP were observed in the CHD group.
  • Specific biomarker profiles differed between the two cities, with variations in IL-8, VEGF, HIF-1α, and Hcy levels.
  • A negative correlation was found between EPC count and hs-CRP in the Lanzhou CHD group.

Conclusions:

  • Reduced EPC levels may be associated with an increased risk of developing CHD.
  • Environmental factors, potentially high altitude, might contribute to EPC reduction and subsequent cytokine dysregulation, promoting CHD.
  • Further research is warranted to elucidate the precise mechanisms linking EPCs, environmental factors, and CHD pathogenesis.
Abstract

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