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Published on: July 12, 2024
Vitamin D Deficiency Harms Patients with Coronary Heart Disease by Enhancing Inflammation
Yongxing Liu1, Wanzhong Peng1, Ya Li1
12nd Department of Cardiology, Cangzhou Central Hospital, Cangzhou, Hebei, China (mainland).
Insights
Vitamin D (VD) deficiency is linked to coronary heart disease (CHD). Low VD levels correlate with increased inflammation and CHD risk, suggesting VD sufficiency is protective against heart disease.
Area of Science:
- Cardiology
- Endocrinology
- Immunology
Background:
- Vitamin D (VD) deficiency and local inflammation are emerging risk factors for coronary heart disease (CHD).
- Understanding the interplay between VD levels and inflammatory markers is crucial for CHD prevention strategies.
Purpose of the Study:
- To investigate the association between serum 25-hydroxyvitamin D (25-OH-VD) levels and coronary heart disease (CHD).
- To explore the role of VD deficiency in modulating inflammatory pathways and lipid profiles in CHD.
Main Methods:
- Compared clinical data and serum levels of 25-OH-VD and inflammatory cytokines (TNF-α, IL-6, IL-8, IL-1β) in 135 CHD patients and 45 controls.
- Utilized a rat model of CHD to examine molecular mechanisms underlying VD deficiency's impact on inflammation and lipid metabolism.
Main Results:
- Serum 25-OH-VD levels were significantly lower in CHD patients and inversely correlated with disease severity.
- Lower 25-OH-VD levels showed a negative correlation with pro-inflammatory cytokines (TNF-α, IL-6, IL-8, IL-1β) in CHD patients.
- In animal models, VD deficiency increased serum TC, TG, and LDL-C, and promoted inflammation via the NF-κB pathway.
Conclusions:
- Serum 25-OH-VD is a protective factor against CHD development.
- VD deficiency exacerbates CHD by enhancing inflammation, potentially through the NF-κB signaling pathway, and negatively impacting lipid profiles.
Abstract:
BACKGROUND Vitamin D (VD) deficiency and local inflammation of plaque are potential new risk factors and prevention goals for coronary heart disease (CHD). MATERIAL AND METHODS This study included 135 CHD patients and 45 chest tightness or chest pain patients (control group). Basic clinical data and serum 25-OH-VD, TNF-α, IL-6, IL-8, and IL-1β of the 2 groups were compared by SPSS 25.0. A CHD rat model was used to explore the potential molecular mechanisms. RESULTS The serum 25-OH-VD level in the control group was significantly higher compared to the CHD group, and decreased with the worsening of the CHD condition. Logistic regression found that serum 25-OH-VD was a protective factor in the occurrence of CHD. In CHD patients, the level of serum 25-OH-VD had a negative correlation with serum TNF-α (r=-0.651, P<0.001), IL-6 (r=-0.457, P<0.001), IL-8 (r=-0.755, P<0.001), and IL-1β (r=-0.628, P<0.001). In animal experiments, VD deficiency enhanced the level of serum TC, TG, and LDL-C. VD deficiency could increase the inflammatory response by upregulating the expression of p65 protein and reducing SIRT1 protein expression in heart tissue, thereby inducing or aggravating the state of CHD. CONCLUSIONS Serum 25-OH-VD was a protective factor in the occurrence of CHD, and VD deficiency could induce or aggravate the state of CHD by enhancing inflammation through the NF-κB pathway.
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