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Published on: January 28, 2020
Expression analysis of inflammatory response-associated genes in coronary artery disease
Nader Ebadi1, Soudeh Ghafouri-Fard1, Mohammad Taheri2
1Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Insights
Inflammation-associated genes, including Antisense noncoding RNA in the INK4 locus (ANRIL), NKILA, and IL-1B, are down-regulated in coronary artery disease (CAD) patients, indicating their role in CAD pathogenesis.
Area of Science:
- Cardiovascular Science
- Molecular Biology
- Immunology
Background:
- Coronary artery disease (CAD) is a leading global cause of mortality.
- Inflammatory processes are implicated in the development of CAD.
Purpose of the Study:
- To compare the expression levels of three inflammation-associated genes: Antisense noncoding RNA in the INK4 locus (ANRIL), NKILA, and IL-1B.
- To investigate the role of these genes in the pathogenesis of CAD.
Main Methods:
- A case-control study design was employed.
- Gene expression levels were compared between CAD patients and matched healthy controls.
- Analysis was stratified by gender.
Main Results:
- ANRIL, NKILA, and IL-1B were significantly down-regulated in CAD patients compared to controls.
- ANRIL and NKILA down-regulation was observed in both male and female CAD patients.
- IL-1B was significantly down-regulated only in female CAD patients.
Conclusions:
- The study demonstrates dysregulation of inflammation-associated genes in the peripheral blood of CAD patients.
- These findings support the involvement of inflammation in the pathogenesis of CAD.
Background:
Coronary artery disease (CAD) is among prominent causes of death throughout the world. Inflammatory processes participate in the pathogenesis of this disorder.
Methods:
In the current case-control study, we compared expression levels of three inflammation-associated genes namely Antisense noncoding RNA in the INK4 locus (ANRIL), NKILA and IL-1B between CAD patients and matched healthy subjects.
Results:
ANRIL, IL-1B and NKILA were significantly down-regulated in CAD patients compared with controls (p values of <.0001, .023 and <.0001, respectively). When evaluating study participants based on their gender, the differences in expression levels of ANRIL and NKILA were significant in both male and female patients compared with the matched controls. However, IL-1B was only down-regulated in female patients compared with female controls.
Conclusion:
Taken together, our study revealed dysregulation of inflammation-associated genes in the peripheral blood of CAD patients and supported the previously suggested role of inflammation in the pathogenesis of CAD.
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