Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The modern way of life contributes to the higher frequency of a complex state medically called metabolic syndrome (MetS), which is an inevitable consequence of several most common diseases of modern civilization. Patients with MetS have three times higher risk of experiencing a heart attack or a stroke and twice higher possibility to die from them. Serbia holds the infamous third place in Europe in mortality from heart disease, just behind Russia and Ukraine. The study explores the correlation of every combination of genotypes of apoE (apolipoprotein E) and LRP1 (low density receptor- related protein 1) genes with presence of MetS, and the connection with each anthropometric and biochemical parameter in both tested groups. Study demonstrates the impact of genotype combinations on the emergence and development of the MetS in Serbia. 63 patients and 30 controls were included in the study, aged from 19 to 65. Each person genotype was determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) profile. Odds ratio (OR) values showed that the presence of apoE e3e4/LRP1 CC genotype combination of genotypes in patients multiplies the chance (7.6 times) for the occurrence of the MetS in comparison to the presence of other genotype combinations. Determining the genetic basis of MetS is one of the necessary steps in the prevention of disease, saving the cost of treatment, and in the design of targeted therapies.
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PMID:Possible synergistic effect of apoE and LRP1 genotypes on metabolic syndrome development in Serbian patients. 3153 2

Inflammation is a pathogenic response to multiple factors, that causes over-activation of different molecules and pro-inflammatory cellular lines. Different behavioral factors and risk factors might enhance the inflammatory stress, and this might cause cardiovascular disease (CVD). CVD is the world's leading cause of morbidity and mortality, and it is represented by hypertension, coronary heart disease, cerebrovascular disease, peripheral vascular disease, heart failure, rheumatic heart disease, congenital heart disease and cardiomyopathies. In this context, inflammation is both a cause and an aggravating factor in CVD, as well as a mediator of its worst prognostic. The mechanisms that link inflammation to CVD are multiple, complex and multi-factorial. To date, the role of inflammation in the genesis and progression of CVD has been extensively analyzed in recent studies. However, in the last decades, new biomarkers are joining the already known inflammatory biomarkers, such as Creactive protein, interleukins, tumor necrosis factor alpha and nitrotyrosine. Among these new biomarkers, we have to report sirtuins, microRNAs, ST2 protein, apolipoprotein E protein, adiponectin, and others. These biomarkers are preferentially expressed locally in the target tissue of inflammation, but also released in peripheral blood and then used as diagnostic and prognostic biomarkers. Indeed, these biomarkers might also predict future adverse cardiovascular events and worse prognosis in patients with CVD. Furthermore, these new inflammatory biomarkers can also be analyzed to evaluate therapeutic efficacy in patients with CVD. Furthermore, this might open up new fields and interesting research concerning the link between inflammation and CVD.
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PMID:Inflammatory Related Cardiovascular Diseases: From Molecular Mechanisms to Therapeutic Targets. 3205 65


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