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Data suggest that, in children with pediatric obesity, lifestyle weight-loss intervention results in down-regulation of serum cardiotrophin-1 (CTF1), interleukin-6 (IL6), and tumor necrosis factor-alpha (TNFA); expression of CTF1, IL6, and TNFA is also down-regulated in peripheral blood mononuclear cells after improvement in adiposity, body mass index, and waist-hip ratio.
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Cardiotrophin-1 levels were not an independent predictor of all-cause mortality in hemodialysis patients.
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We identify the cytokine cardiotrophin 1 (CT1) as a factor capable of recapitulating the key features of physiologic growth of the heart including transient and reversible hypertrophy of the myocardium, and stimulation of cardiomyocyte-derived angiogenic signals leading to increased vascularity
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a transcriptional factor, Myc-associated zinc finger protein (MAZ), plays an important role in ADAM10 transcription in response to CT-1 in neural stem/progenitor cells.
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CT-1 was found to be associated with Tn-I, which is used to detect myocardial damage after OPCAB surgery. CT-1 may also be used to detect myocardial damage.
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non-diabetic subjects who were overweight or obesity had significantly lower cardiotrophin-1 concentrations than those with normal weight, and both obesity and being overweight were inversely associated with cardiotrophin-1 levels.
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This paper will review many aspects of CT-1 physiological role in several organs and discuss data for consideration in therapeutic approaches.
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biliary epithelium-derived CT-1 may exert a profibrogenic potential in PCLD.
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Data show that cardiotrophin-1 is positively related to brachial-ankle pulse-wave velocity (baPWV) independent of traditional cardiometabolic risk factors for arterial stiffness.
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this study, even though preliminary and awaiting further confirmation by independent replication, provides first evidence that common genetic variation in CTF1 could contribute to insulin sensitivity in humans.
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Study correlates CT-1 levels with ambulatory and central BP, as well as with pulse wave velocity in patients with essential hypertension.
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CT-1 is differentially induced in the myocardium of infants with congenital cardiac defects depending on hypoxemia, and may mediate myocardial hypertrophy and dysfunction.
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Subjects with impaired glucose tolerance (IGT) and newly diagnosed diabetes (NDD) have significantly higher CT-1 concentrations than those with normal glucose tolerance. IGT and NDD are positively associated with CT-1 concentrations.
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exaggerated cardiomyocyte production of cardiotrophin-1 in response to increased left ventricular end-diastolic stress may contribute to fibrosis through stimulation of fibroblasts in heart failure of hypertensive origin.
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A reduction in serum CT-1 levels after a WL program.
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CT-1 induces the proteolytic potential in human aortic endothelial cells by upregulating MMP-1 expression.
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Cardiotrophin-1 may serve as both a biomarker of left ventricular hypertrophy and dysfunction in hypertensive patients, and is potential target for therapies aimed to prevent and treat hypertensive heart disease beyond blood pressure control.
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Hypoxia increased cardiotrophin-1 levels in cardiac cells through a direct regulation of CT-1 promoter by HIF-1alpha, protecting cells from apoptosis.
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CT-1 treatment of myofibroblasts was associated with increased phosphorylation of myosin light chain kinase via myosin light chain kinase to induce cell migration.
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the 1742(C/G) polymorphism of the human CT-1 gene is associated with LVH in hypertension, and the GG genotype may have a protective role