Coronary artery disease (CAD) is the leading cause of death worldwide and it is basically caused by atherosclerosis. The atherosclerotic process includes complex events and each one involves a specific biological pathway and different genes. According to World Health Organization report, Cardiovascular diseases will be the largest cause of death and disability by 2020, with an estimated 2.6 million Indians predicted to die due to CAD predominantly with myocardial infarction. Genetic factors are estimated to contribute 30-60% of the CAD risk. The aim of this study is to investigate the association of COL4A1 and CD14 genes polymorphism with CAD. This study included 345 subjects, 185 CAD cases and 160 healthy controls. Single-nucleotide polymorphisms were evaluated by polymerase chain reaction and restriction fragment length polymorphism. Alleles and genotype frequencies between cases and controls were compared using χ and Student's t tests. Odds ratios and 95% confidence intervals were calculated by logistic regression to assess the relative association between disease and genotypes. In this study, CD14 (rs2569190), CC (P = 0.008) genotypes, and C allele (P = 0.007) were found to be a positive risk factor, while TT genotype (P = 0.045) and T allele (P = 0.007) as negative risk factor for CAD. Significant differences were not observed in COL4A1 (rs605143 and rs565470) gene polymorphism with CAD. It seems that CD14 gene polymorphism might be associated with the risk of CAD, whereas COL4A1 gene polymorphism was not found to confer any risk of CAD.
In Fig-1 shown that, in the primary phase of glycosylated hemoglobin formation, hemoglobin and blood glucose react reversibly to the aldimine. In the irreversible secondary phase, aldimina gradually becomes a stable 6 form of ketoamine. The main sites of hemoglobin glycosylation are in the order of their prevalence β-Val-1, β-Lys-66 and α-Lis-61. Normal adult hemoglobin
There are about 40% of patients with type 1 and type 2 diabetes will develop diabetic nephropathy (DN), resulting in chronic kidney disease and potential organ failure. During the progression and development of DN, chronic elevated blood glucose (hyperglycaemia) together with glomerular hypertension leads to renal inflammation, progressive glomerulosclerosis and tubulointerstitial fibrosis resulting in organ failure. Genetic variants at a biomarker level could allow the detection of those individuals at high risk for diabetic nephropathy which could thus help in the treatment, diagnosis and early prevention of the disease. Current genome-wide relationship scans have recognized a number of chromosomal regions that possible include diabetic nephropathy susceptibility genes, and association analyses have evaluated positional applicant genes under these relation peaks. The possibility of increasing diabetic nephropathy is recovered several times by inheriting risk alleles at susceptibility loci of dissimilar genes like GST (glutathione-Stransferase), TCF (Transcription factor), ELMO1 (Engulfment and Cell Motility 1), IL-10 (Interleukin-10) and TRPC1 (transient receptor potential channel 1). The identification of these genetic variants at a biomarker level could thus, allow the detection of those individuals at high risk for diabetic nephropathy which could thus help in the treatment, diagnosis and early prevention of the disease.
Diabetes type II is an autoimmune disorder of multiple etiologies that is basically due to deregulation of blood glucose homeostatis, thus causing hyperglycemia accompanied by various other disturbances of carbohydrates, fat and protein metabolism. Broad classification of these diabetic complications involves two major groups-microvascular which includes retinopathy (leading to blindness), nephropathy (leading to renal failure) and neuropathy (leading to nerve damage) and macrovascular, including cardiovascular complexity and peripheral vascular disease. Diabetic retinopathy (DR) is a microangiopathy that induces optical complications in a diabetic subject that leads to acquired blindness in young adults due to high susceptibility of cellular components of retina towards the hyperglycemic environment. A large number of protein coding genes and some non-coding RNAs (ncRNAs) are reported to be involved, among which miRNAs are a small group of ncRNAs that are broadly studied to understand the pathology of the disease. Therefore, the functions and initiation of miRNAs could be regulated as their variation is allied with a broad array of functional defects, including incurable conditions. This review focuses on the molecular mechanisms of miRNA in response to DR.
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