MicroRNAs and Cardiovascular Disease in Diabetes Mellitus

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Term Occurence Count Dictionary
obesity 2 endocrinologydiseases
pioglitazone 2 endocrinologydiseasesdrugs
Insulin 1 endocrinologydiseasesdrugs
diabetes mellitus 2 endocrinologydiseases
enalapril 1 endocrinologydiseasesdrugs
hyperglycemia 8 endocrinologydiseases
metformin 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 20743 Besides, it was found that microRNAs control the insulin signal transduction pathways in target tissues. Insulin resistance refers to the failure of target tissues, including the liver, skeletal muscle, and adipose
enalapril 13095 secretion in VSMCs, which inhibited miR-145 expression under HG conditions. Furthermore, the addition of enalapril at dihydrate and valsartan, an Ang II receptor antagonist, significantly upregulated miR-145 expression
metformin 5785 activates eNOS and results in impaired angiogenesis. Moreover, treatment with miR-34a inhibitor or metformin downregulated miR-34a expression and upregulated SIRT1 expression, indicating that the hyperglycemia-induced
pioglitazone 25331 decreases in smooth muscle cell migration and proliferation when patients with T2DM were treated with pioglitazone [[49]]. A subsequent prospective study showed that pioglitazone significantly decreased neointimal hyperplasia
pioglitazone 25395 patients with T2DM were treated with pioglitazone [[49]]. A subsequent prospective study showed that pioglitazone significantly decreased neointimal hyperplasia (NIH), accompanied by increases in circulating miR-24.
Select Disease Character Offset Disease Term Instance
diabetes mellitus 548 date (epub): 2/2017AbstractCardiovascular disease (CVD) is the major macrovascular complication of diabetes mellitus . Recently, although CVD morbidity and mortality have decreased as a result of comprehensive control
diabetes mellitus 1346 macrophage and platelet activation, lipid metabolism abnormality, and cardiomyocyte repolarization in diabetes mellitus . We also review the progress of microRNAs as potential biomarkers and therapeutic targets of CVD in
hyperglycemia 1741 elevated blood glucose levels as well as abnormal fat and protein metabolism [[1], [2]]. Long-term hyperglycemia can result in both microvascular and macrovascular complications, of which cardiovascular disease (CVD)
hyperglycemia 3897 diabetes. Both in vivo and in vitro studies have shown that the abnormal expression of microRNAs induced by hyperglycemia causes endothelial cell, vascular smooth muscle cell (VSMC), platelet and macrophage dysfunction, and
hyperglycemia 4800 and lipid accumulation. It has been confirmed that the abnormal expression of microRNAs induced by hyperglycemia is involved in this abnormality. Furthermore, it appears that CVD is aggravated by arrhythmia caused
hyperglycemia 5882 or metformin downregulated miR-34a expression and upregulated SIRT1 expression, indicating that the hyperglycemia -induced modulation of SIRT1 levels and posttranslational modification of eNOS took place through a miR-34a-dependent
hyperglycemia 7516 reduced cell migration and formation of microvasculature structure. dfECFCs treated with HG to mimic hyperglycemia or with HG combined with low growth factor (LGF) conditions (HG/LGF) to mimic the poorest progression
hyperglycemia 18287 membrane ion channels is an important structural basis of arrhythmia. Li et al. [[30]] demonstrated that hyperglycemia led to electrophysiological change in cardiac progenitor cells (CPCs), which play an important role
hyperglycemia 29590 and effective management.Figure 1Schematic overview of the role of microRNAs in endothelial cells in hyperglycemia .Figure 2Schematic overview of the role of microRNAs in vascular smooth muscle cell in hyperglycemia
hyperglycemia 29690 hyperglycemia.Figure 2Schematic overview of the role of microRNAs in vascular smooth muscle cell in hyperglycemia or diabetes.Figure 3MicroRNAs involved in lipid metabolism
obesity 2029 also an independent risk factor for CVD, excluding other risk factors such as age, hypertension, and obesity [[3], [4]]. Most patients with CVD often have abnormal glucose metabolism, meaning diabetes and CVD
obesity 17664 sensitivity, decreased hepatic glucose production, and decreased fatty acid synthesis, thereby preventing obesity -induced metabolic complications. Conversely, silencing endogenous miR-26a in conventional diet-fed mice

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