Vitamin D receptor polymorphisms and diseases.

The interactions of chemokines with their G protein-coupled receptors promote the migration of leukocytes during normal immune function and as a key aspect of the inflammatory response to tissue injury or infection. This review summarizes the major cellular and biochemical mechanisms by which the interactions of chemokines with chemokine receptors are regulated, including: selective and competitive binding interactions; genetic polymorphisms; mRNA splice variation; variation of expression, degradation and localization; down-regulation by atypical (decoy) receptors; interactions with cell-surface glycosaminoglycans; post-translational modifications; oligomerization; alternative signaling responses; and binding to natural or pharmacological inhibitors.

Mechanisms of regulation of the chemokine-receptor network

Aims: To determine the roles of vitamin D receptor (VDR) in ischemia/reperfusion-induced myocardial injury and to investigate the underlying mechanisms involved. Results: The endogenous VDR expression was detected in the mouse heart, and myocardial ischemia/reperfusion (MI/R) upregulated VDR expression. Activation of VDR by natural and synthetic agonists reduced myocardial infarct size and improved cardiac function. Mechanistically, VDR activation inhibited endoplasmic reticulum (ER) stress (determined by the reduction of CCAAT/enhancer-binding protein homologous protein expression and caspase-12 activation), attenuated mitochondrial impairment (determined by the decrease of mitochondrial cytochrome c release and caspase-9 activation), and reduced cardiomyocyte apoptosis. Furthermore, VDR activation significantly inhibited MI/R-induced autophagy dysfunction (determined by the inhibition of Beclin 1 over-activation, the reduction of autophagosomes, the LC3-II/LC3-I ratio, p62 protein abundance, an...

Vitamin D Receptor Activation Protects Against Myocardial Reperfusion Injury Through Inhibition of Apoptosis and Modulation of Autophagy

Introduction: Both cardiovascular disease and osteoporosis are important causes of morbidity and mortality in the elderly. The co-occurrence of cardiovascular disease and osteoporosis prompted us to review the evidence of an association between cardiovascular (CV) disease and osteoporosis and potential shared common pathophysiological mechanisms. Methods: A systematic literature search (Medline, Pubmed and Embase) was conducted to identify all clinical studies that investigated the association between cardiovascular disease and osteoporosis. Relevant studies were screened for quality according to guidelines as proposed by the Dutch Cochrane Centre and evidence was summarized. Results: Seventy studies were included in this review. Due to a large heterogeneity in study population, design and outcome measures a formal meta-analysis was not possible. Six of the highest ranked studies (mean n = 2,000) showed that individuals with prevalent subclinical CV disease had higher risk for increased bone loss and fractures during follow-up compared to persons without CV disease (range of reported risk: hazard ratio (HR) 1.5; odds ratio (OR) 2.3 to 3.0). The largest study (n = 31,936) reported a more than four times higher risk in women and more than six times higher risk in men. There is moderate evidence that individuals with low bone mass had higher CV mortality rates and incident CV events than subjects with normal bone mass (risk rates 1.2 to 1.4). Although the shared common pathophysiological mechanisms are not fully elucidated, the most important factors that might explain this association appear to be, besides age, estrogen deficiency and inflammation. Conclusions: The current evidence indicates that individuals with prevalent subclinical CV disease are at increased risk for bone loss and subsequent fractures. Presently no firm conclusions can be drawn as to what extent low bone mineral density might be associated with increased cardiovascular risk.

/pdf/sub-clinical-cardiovascular-disease-is-associated-with-2mf3rtejvu.pdf

(Sub)clinical cardiovascular disease is associated with increased bone loss and fracture risk; a systematic review of the association between cardiovascular disease and osteoporosis

Calcific aortic valve stenosis is the result of regulated cell processes. The histological hallmarks are inflammation and a remodelling of the extracellular matrix leading to bone formation. In the last 15 years the view has changed from it being an unmodifiable degenerative disease to an active biological process regulated by highly conserved ubiquitous cellular pathways. Many mechanisms and risk factors are the same as in atherosclerosis. Thus, statins and angiotensin II antagonists seemed promising treatment options. However, clinical trials failed to support this. This review describes the current understanding of major molecular mechanisms and discusses their role in clinical practice and possible therapy.

https://heart.bmj.com/content/heartjnl/95/8/616.full.pdf?95%2F8%2F616=

Aortic valve calcification: basic science to clinical practice.

http://www.ujaen.es/investiga/inmunoge/gmo/seminarios/SEMINARIOS%20GENMOL/POLYMORPHISMS_CCR2_VDR_IL6_infarto.pdf

Additive effects of the chemokine receptor 2, vitamin D receptor, interleukin-6 polymorphisms and cardiovascular risk factors on the prevalence of myocardial infarction in patients below 65 years.

Objectives: To analyse the association of APOE alleles with aortic stenosis (AS) in a large study population. Methods: Patients with AS (n  =  538) and a control group of the same age without heart disease (n  =  536) were recruited. Left heart catheterisation was performed and mean gradient, aortic valve area, presence of stenotic coronary artery disease (CAD) and cardiovascular risk factors (hypercholesterolaemia, hypertension, smoking, diabetes mellitus and family history of CAD) were assessed. The frequency of the APOE major alleles e2, e3 and e4 was assessed by genotyping the polymorphisms APOE334 and APOE472 with a 5′ exonuclease assay (TaqMan). Results: Mean gradient across the aortic valve in cases was 50 (SD 20) mm Hg corresponding to a mean aortic valve area of 0.84 (SD 0.34) cm 2 . 270 patients with AS had stenotic CAD. Among patients with AS, the prevalence of hypercholesterolaemia (64% v 40%, p v 27%, p v 17%, p v 21%, p ⩽ 0.05), and male sex (65% v 44%, p v 94 (17.5%); APOE e3: 319 (59.3%) v 332 (61.9%); APOE e4: 115 (21.3%) v 110 (20.5%); all p > 0.10). Conclusion: APOE e4 is not associated with AS, reflecting the different genetic backgrounds of CAD and AS.

https://heart.bmj.com/content/heartjnl/92/10/1463.full.pdf?related-urls=yes&legid=heartjnl%3B92/10/1463

APOE alleles are not associated with calcific aortic stenosis.

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Additive effects of the chemokine receptor 2, vitamin D receptor, interleukin-6 polymorphisms and cardiovascular risk factors on the prevalence of myocardial infarction in patients below 65 years.

APOE alleles are not associated with calcific aortic stenosis.