Find in Library

Vitamin D deficiency is highly prevalent worldwide. It has been associated with heart failure (HF) given its immunoregulatory functions. In-vitro and animal models have shown protective roles through mechanisms involving procollagen-1, JNK2, calcineurin/NFAT, NF-&#954;B, MAPK, Th1, Th2, Th17, cytokines, cholesterol-efflux, oxLDL, and GLUT4, among others. A 12-month follow-up in HF patients showed a high prevalence of vitamin D deficiency, with no seasonal variation (64.7&#8722;82.4%). A positive correlation between serum 25(OH)D concentration and dietary intake of vitamin D-rich foods was found. A significant inverse correlation with IL-1&#946; (<i>R</i> = &#8722;0.78), TNF-&#945; (<i>R</i> = &#8722;0.53), IL-6 (<i>R</i> = &#8722;0.42), IL-8 (R = &#8722;0.41), IL-17A (<i>R</i> = &#8722;0.31), LDL-cholesterol (<i>R</i> = &#8722;0.51), Apo-B (<i>R</i> = &#8722;0.57), total-cholesterol (<i>R</i> = &#8722;0.48), and triglycerides (<i>R</i> = &#8722;0.32) was shown. Cluster analysis demonstrated that patients from cluster three, with the lowest 25(OH)D levels, presented the lowermost vitamin D intake, IL-10 (1.0 &#177; 0.9 pg/mL), and IL-12p70 (0.5 &#177; 0.4 pg/mL), but the highest TNF-&#945; (9.1 &#177; 3.5 pg/mL), IL-8 (55.6 &#177; 117.1 pg/mL), IL-17A (3.5 &#177; 2.0 pg/mL), total-cholesterol (193.9 &#177; 61.4 mg/dL), LDL-cholesterol (127.7 &#177; 58.2 mg/dL), and Apo-B (101.4 &#177; 33.4 mg/dL) levels, compared with patients from cluster one. Although the role of vitamin D in the pathogenesis of HF in humans is still uncertain, we applied the molecular mechanisms of in-vitro and animal models to explain our findings. Vitamin D deficiency might contribute to inflammation, remodeling, fibrosis, and atherosclerosis in patients with HF.