Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary collateral vessels reduce the damage of ischemic myocardium after coronary obstruction. Recently, vascular endothelial growth factor (VEGF) has been shown to increase vascular permeability and enhance the endothelial cell growth, leading to neoangiogenesis. VEGF has been reported to be upregulated in some neoplasms with endothelial proliferation, such as glioblastoma and vascularised adenocarcinoma. However, the expression and role of VEGF in human heart and those in its diseased condition have not been investigated. To elucidate its pathophysiological role, we studied the transcription and distribution of VEGF mRNA in normal human and myocardial infarcted hearts. Samples were obtained from 15 autopsy cases with and without ischemic heart disease. VEGF mRNA transcription was examined by using RT-PCR and Southern blot analysis. In all cases VEGF mRNA was detected in atrias, ventricles and valves. The amounts of each VEGF subtypes in cardiomyocytes were different from those in valves. By in situ hybridization method, VEGF mRNA was found in cytoplasm of normal cardiomyocyte but not in the vessels. However, in the cases of acute myocardial infarction, VEGF mRNA was detected in vascular smooth muscle cells of arterioles around the coagulation necrosis of the infarction as well as in mononuclear cells which infiltrated in the granulation tissues. In contrast, VEGF mRNA signals in cardiomyocyte around the necrosis were as much as those in the normal cardiomyocyte in non-diseased areas. By immunohistochemical studies, the mononuclear cells were supposed to be macrophages. This study suggests that VEGF could play an important role in neovascularization in acute myocardial infarction, and suggests that VEGF may have some favorable effect on infarcted myocardium.
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PMID:[The expression and the role of vascular endothelial growth factor (VEGF) in human normal and myocardial infarcted heart]. 795 3

The present review aimed to present the research highlights on C1q/TNF-related protein 1 (CTRP1), a member of the recently discovered family of highly conserved adiponectin paralog proteins, C1q tumor necrosis factor-related proteins. CTRP1 plays an important role in regulating body energy homeostasis and sensitivity to insulin. Studies on animal models have shown that it lowers the concentration of glucose. Elevated concentrations of CTRP1 reduce weight gain and diet-induced insulin resistance. CTRP1 limits the extent of ischemia-reperfusion injury in acute myocardial infarction. It inhibits platelet aggregation by blocking von Willebrand factor binding to collagen. In patients with chronic kidney disease, an increase in CTRP1 levels is associated with a lesser degree of disease progression. CTRP1 stimulates aldosterone synthesis in the adrenal cortex by affecting aldosterone synthase expression. In dehydration, an increase in CTRP1 concentration helps to maintain normotension. It participates in processes related to the proliferation and maturation of chondrocytes. It also promotes atherosclerosis, and a surge in its concentration is correlated with a higher cardiovascular risk in patients with coronary atherosclerosis. In vascular smooth muscle cells, it induces the expression of proinflammatory cytokines. An increase in CTRP1 levels is correlated with the progression of the neoplastic process in patients with glioblastoma.
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PMID:C1q/TNF-related Protein 1, a Multifunctional Adipokine: An Overview of Current Data. 3259 Oct 91