Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P39060 (endostatin)
 2,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute ischemia is a well-known inductor of extracellular matrix (ECM) remodeling, which leads to the development of congestive heart failure and is associated with left ventricular dilatation. Here we investigate the timecourse of ECM processing with release of endostatin (ES) and other low-molecular-weight fragments during early ischemia-reperfusion of the heart. In this blinded study, 30 pigs were randomized to 60 min of global myocardial ischemia at either 4 or 37 degrees C or served as control. Five transmyocardial tissue samples were collected at baseline and after ischemia within 150 min of reperfusion. Collagen XVIII cleavage products of 10-75 kDa including ES (25 kDa) were analyzed using the Western blot and ELISA method, and creatin kinase as marker of myocardial injury was determined in samples collected from the coronary sinus. We demonstrate that processing of the extracellular matrix protein collagen XVIII starts during early reperfusion, as we observed a significantly increased expression of cleavage products at 10 and 75 kDa as well as ES at 150 min of normothermic ischemia-reperfusion. We further demonstrate a differential processing of collagen XVIII depending on temperature conditions during myocardial ischemia, as an increase in cleavage products was observed after normothermic ischemia only; however, expression of ES and other fragments remained unchanged after hypothermic ischemia-reperfusion and in controls. In conclusion, this blinded study first demonstrated that processing of extracellular matrix started early after ischemia-reperfusion and depends on temperature conditions. These findings may contribute to a broader understanding of matrix processing after ischemia-reperfusion.
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PMID:Ischemia-reperfusion injury activates early extracellular matrix processing and expression of endostatin in the heart with differential effects of temperature. 1925

Aim of the study was to assess effect of myocardial revascularization on levels of factors of angiogenesis in early and remote period after intervention. Main group comprised 228 patients with ischemic heart disease (n=228, 194 men, 34 women, mean age 57+/-8.7 years). Coronary bypass surgery was carried out in 29 patients while other 199 were subjected to percutaneous coronary intervention (PCI). Analysis of data was performed in the group as a whole and in 2 subgroups distinguished in dependence on type of invasive treatment. Levels of factors of angiogenesis - vascular endothelial growth factor (VEGF), transforming growth factor beta (TGFbeta), and endostatin - were measured before, in 6 days, and 6 months after invasive treatment. Compared with healthy persons patients with IHD had significantly higher level of VEGF and significantly lower levels of TGFbeta and endostatin. On day 6 after revascularization in the group as a whole level of VEGF insignificantly rose while level of TGFbeta insignificantly decreased. In 6 months after invasive treatment significant lowering of VEGF level and significant increase of TGFbeta was noted. Endostatin level was measured at baseline and in 6 months after invasive treatment. Significant elevation of endostatin level took place after 6 months. Thus PCI and coronary bypass surgery lead to lowering of VEGF level and elevation of levels of TGFbeta in 6 days after intervention. In remote period reverse dynamics was observed: of VEGF level rose and those of TGFbeta and endostatin increased.
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PMID:[Effect of myocardial revascularization on dynamics of factors of angiogenesis in patients with ischemic heart disease]. 2003 74

Concerns have arisen regarding the risk of ischemic heart disease with the novel antiangiogenic agent bevacizumab, a recombinant humanised monoclonal antibody to the vascular endothelial growth factor that is widely used in cancer treatment. Currently, the role of bevacizumab in ischemic heart disease is controversial. This meta-analysis was therefore performed to assess the overall risk of ischemic heart disease associated with the use of bevacizumab. The databases of PubMed, EMBASE and Web of Science were searched for English language studies of randomised controlled trials comparing bevacizumab with control therapy published through October 25, 2012. Summary incidence rates, relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random-effects or fixed-effects models based on the heterogeneity of the included studies. A total of 4,617 patients from 7 randomised controlled trials were identified and included for analysis. Among those patients receiving bevacizumab, the summary incidence of ischemic heart disease was 1.0% (95% CI, 0.6%-1.4%). Patients treated with bevacizumab had a significantly increased risk of ischemic heart disease with an RR of 2.49 (95% CI, 1.37-4.52) compared with controls. In addition, both high doses and low doses of bevacizumab increased the risk of cardiac ischemia (low dose at 2.5 mg/kg per week: RR, 2.14 [95% CI, 1.09-4.19]; high dose at 5 mg/kg per week: RR, 4.81 [95% CI, 1.03-22.42]). Bevacizumab was also found to significantly increase the risk of cardiac ischemia in patients with colorectal cancer (RR, 2.13; 95% CI, 1.11-4.06) compared with controls. This meta-analysis shows the use of bevacizumab was associated with an increased risk of developing ischemic heart disease in colorectal cancer patients receiving this drug. Our conclusions are limited by the available data. Further evaluations of high-quality RCTs are needed.
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PMID:Angiogenesis inhibitor bevacizumab increases the risk of ischemic heart disease associated with chemotherapy: a meta-analysis. 2381 62