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DUSP1 Is a Potential Marker of Chronic Inflammation in Arabs with Cardiovascular Diseases

Abdelkrim Khadir1, Sina Kavalakatt1, Mohammed Dehbi2

  • 1Research Division, Dasman Diabetes Institute, Kuwait.

Disease Markers
|January 17, 2019
PubMed

Insights

Dual-specificity phosphatase 1 (DUSP1) may predict chronic inflammation and residual cardiovascular disease (CVD) risk. High-sensitivity C-reactive protein (hsCRP) association with CVD is linked to obesity, not inflammation.

Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Medicine

Background:

  • Cardiovascular disease (CVD) poses ongoing risks despite conventional treatments, potentially linked to chronic inflammation.
  • Epidemiological studies suggest a correlation between low-grade inflammatory markers and recurrent CVD events.
  • This study investigates plasma dual-specificity phosphatase 1 (DUSP1) as a potential inflammatory marker in CVD patients.

Purpose of the Study:

  • To assess plasma DUSP1 levels in CVD patients compared to controls.
  • To compare DUSP1 with established markers: high-sensitivity C-reactive protein (hsCRP) and oxidized low-density lipoprotein (oxLDL).
  • To explore the association of these markers with conventional CVD risk factors.

Main Methods:

  • A cohort of 207 CVD patients and 70 controls in Kuwait was studied.
  • Anthropometric and biochemical parameters were measured.
  • Plasma levels of DUSP1, oxLDL, and hsCRP were quantified using enzyme-linked immunosorbent assay kits.

Main Results:

  • Plasma DUSP1 and hsCRP levels were significantly higher in CVD cases, while oxLDL was lower.
  • Multivariate analysis revealed independent associations of DUSP1 and hsCRP with CVD, indicating increased risk.
  • DUSP1 associated with CVD independently of statin use and diabetes, whereas hsCRP correlated with obesity markers.

Conclusions:

  • Circulating DUSP1 may serve as a predictor of chronic subclinical inflammation and residual CVD risk.
  • The association between hsCRP and CVD appears primarily mediated by adiposity-related factors.
Abstract

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