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)

Kawasaki disease (KD) is a multisystemic vasculitis that often includes coronary artery involvement. The serum levels of matrix metalloproteinase (MMP)-3 and -9 are significantly elevated in KD patients, and polymorphisms in the genes encoding MMP-3 and MMP-9 have been associated with the susceptibility, severity, and progression of atherosclerosis and aneurysm. However, the association between MMP-3 gene polymorphisms and development of aneurysm is somewhat controversial in a number of diseases. Ninety-seven children with KD and 194 children with congenital heart disease (CHD) were included in this study. Echocardiography was used to examine all children in the KD group for coronary artery aneurysm. Genotyping of the MMP-3 (-439C/G) promoter polymorphism was performed using the single-base extension method, and serum MMP-3 levels were estimated using the sandwich enzyme immunoassay method. There was no significant difference in MMP-3 (-439C/G) genotypes between KD and control groups. There was no association between this MMP-3 polymorphism and development of coronary aneurysm in KD. Serum MMP-3 levels were significantly higher in KD patients compared to control subjects. Among the KD patients, serum MMP-3 levels were higher in children with genotypes CG+GG compared to the CC group, but this difference was not significant. Although further large-scale studies will be required to fully examine the relationship between MMP-3 gene polymorphisms and coronary artery lesions (CAL) in KD, the present findings suggest that while MMP-3 may play a role in the pathogenesis of KD, there is no apparent association between CAL and the MMP-3 (-439C/G) gene polymorphism in Korean children with KD.
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PMID:Association of the matrix metalloproteinase-3 (-439C/G) promoter polymorphism with Kawasaki disease in Korean children. 1881 May 83

When challenged by hemodynamic stress, aging hearts respond differently to young hearts. Preclinical models of heart disease should take into account the effects of age. However, in the transverse aortic constriction (TAC) model of pressure-overload cardiomyopathy, the larger aorta of aging mice has not previously been taken into account. First, we studied the aortic size in mice, and found that the aortic cross-sectional area (CSA) is 28% larger in aging mice than in young adult mice (P=0.001). We then performed TAC to make the same proportional reduction in CSA in young and aging mice. This produced the same pressure gradient across the constriction and the same rise in B-type natriuretic peptide expression. Young mice showed acute deterioration in systolic function assessed by pressure-volume loops, progressive LV remodeling on echocardiography, and a 50% mortality at 12 weeks post-TAC. In contrast, aging mice showed no acute deterioration in systolic function, much less ventricular remodeling and were protected from death. Aging mice also showed significantly increased levels of matrix metalloproteinase-3 (MMP-3; 3.2 fold increase, P<0.001) and MMP-12 (1.5-fold increase, P<0.001), which were not seen in young mice. Expression of tissue inhibitor of MMP-1 (TIMP-1) increased 8.6-fold in aging hearts vs 4.3-fold in young hearts (P<0.01). In conclusion, following size-appropriate TAC, aging mice exhibit less LV remodeling and lower mortality than young adult mice. This is associated with induction of protective ECM changes.
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PMID:Aging is protective against pressure overload cardiomyopathy via adaptive extracellular matrix remodeling. 2869 53

Therapeutic hypothermia during cardiac surgery has been widely used for neuroprotection and to attenuate the systemic inflammatory response due to cardiopulmonary bypass (CPB). Experimental data suggest that cold-shock protein RNA-binding motif 3 (RBM3), which is induced in response to hypothermia, plays a key role in hypothermia-induced organ protection. To date, investigation on RBM3 has been performed exclusively in vitro or in animal models, and the detection and regulation of RBM3 in human blood has not been investigated until now. The aim of this study was to investigate the level of RBM3 protein and cytokine expression profile involved in the inflammatory response in patients with congenital heart disease undergoing cardiac surgery involving CPB and therapeutic hypothermia. A single-center prospective trial with 23 patients undergoing cardiac surgery with CPB was performed. RBM3 protein was quantified in blood serum samples collected from patients and healthy individuals employing a new developed enzyme-linked immunosorbent assay. Cytokine levels were analyzed from dry blood spot samples using a Quanterix Simoa Immunoassay. For the first time, RBM3 protein was detected in blood samples of patients with congenital heart disease undergoing cardiac surgery. Hereby, RBM3 protein concentrations were significantly elevated in patients after cardiac surgery with CPB and mild hypothermia as compared with pre-surgery levels. Moreover, a complex immune reaction with significant induction of pro-inflammatory cytokines (interleukin [IL]-1 beta, IL-6, IL-8, IL-16, IL-18, monocyte chemotactic protein 1, CC-chemokine ligand [CCL]3, CCL4, intercellular adhesion molecule-1) in response to CPB was detected. Significantly elevated vascular endothelial growth factor and matrix metallopeptidase 3 concentrations reflecting ischemia/reperfusion-induced injury were observed 24 hours after weaning from CPB. The use of CPB is still associated with a complex inflammatory response. RBM3 protein is measurable in blood samples of patients with significantly higher concentrations after cardiac surgery with CPB and mild-to-moderate hypothermia. RBM3 is a new candidate as a biomarker for therapeutic hypothermia and a possible new therapeutic target for organ protection.
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PMID:A Prospective Clinical Trial Measuring the Effects of Cardiopulmonary Bypass Under Mild Hypothermia on the Inflammatory Response and Regulation of Cold-Shock Protein RNA-Binding Motif 3. 3097 5