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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.
Cardiotrophin-1 levels were not an independent predictor of all-cause mortality in hemodialysis patients.
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
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.
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.
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.
This paper will review many aspects of CT-1 physiological role in several organs and discuss data for consideration in therapeutic approaches.
biliary epithelium-derived CT-1 may exert a profibrogenic potential in PCLD.
Data show that cardiotrophin-1 is positively related to brachial-ankle pulse-wave velocity (baPWV) independent of traditional cardiometabolic risk factors for arterial stiffness.
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.
Study correlates CT-1 levels with ambulatory and central BP, as well as with pulse wave velocity in patients with essential hypertension.
CT-1 is differentially induced in the myocardium of infants with congenital cardiac defects depending on hypoxemia, and may mediate myocardial hypertrophy and dysfunction.
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.
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.
A reduction in serum CT-1 levels after a WL program.
CT-1 induces the proteolytic potential in human aortic endothelial cells by upregulating MMP-1 expression.
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.
Hypoxia increased cardiotrophin-1 levels in cardiac cells through a direct regulation of CT-1 promoter by HIF-1alpha, protecting cells from apoptosis.
CT-1 treatment of myofibroblasts was associated with increased phosphorylation of myosin light chain kinase via myosin light chain kinase to induce cell migration.
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
These results suggest that CT-1 may be a potent candidate for the early prevention and treatment of Alzheimer disease.
Identify cardiotrophin-1 as a powerful cytokine promoting mesenchymal stromal cell engraftment and thus improving cell therapy of the infarcted myocardium.
CT-1 mRNA levels in adipose tissue showed significant circadian fluctuations in young WT mice. Clock genes displayed a circadian rhythm in adipose tissue of both wild-type (WT) and CT-1-/- mice. However, the pattern was altered in CT-1-/- mice toward a lower percentage of the rhythm or lower amplitude, especially for Bmal1 and Clock.
Cardiotrophin-1 modulates the production of adipokines in vitro and in vivo, suggesting that the regulation of the secretory function of adipocytes could be involved in the metabolic actions of this cytokine.
Nuclear translocation of CT-1 regulates cardiomyogenesis of ES cells and involves calcium, NO, ROS as well as CT-1 regulated signaling pathways.
Data suggest that Ctf1 up-regulates lipolysis in white adipocytes via 1) induction of perilipin, 2) activation of hormone sensitive lipase (via phosphorylation by PKA), and 3) inactivation of adipose triglyceride lipase (via up-regulation of G0S2).
Cardiotrophin-1 (CT-1) is a hepatoprotective cytokine that modulates fat and glucose metabolism. Here we analyzed the changes in hepatic fat stores induced by recombinant CT-1 and its therapeutic potential in non-alcoholic fatty liver disease.
The transgenic expression of CTF1 brought about a marked improvement on cognitive functioning in the APPswe/PS1dE9 transgenic mouse model of Alzheimer's disease.
CT-1 improves beta cell function and survival, and protects mice against STZ-induced diabetes
CT-1 may be a major regulator of arterial stiffness with a major impact on the aging process.
Data suggest a key role for CT-1 in cardiac remodeling induced by aldosterone independent of changes in blood pressure levels.
We conclude that CT-1 is a master regulator of fat and glucose metabolism with potential applications for treatment of obesity and insulin resistance.
Treatment of embryoid bodies grown from pluripotent murine embryonic stem (ES) cells with cardiotrophin 1 significantly stimulated cardiomyogenesis and increased nuclear expression of the proliferation marker Ki-67.
In cntf/lif/ct-1 triple-knock-out mice, various degrees of muscle fiber type grouping are found, showing that denervation & reinnervation had occurred. CNTF, LIF, & CT-1 have distinct functions for motoneuron survival and function.
The embryonic neurons of mice regulate the onset of cortical gliogenesis via cardiotrophin-1.
In embryonic deficient mice, preganglionic sympathetic neurons were reduced.
Induction of interleukin-6 mRNA after infarct was significantly abrogated in CT-1 null mice compared to wild-type mice
CT-1 is an essential endogenous defense of the liver against ischemia-reperfusion injury and is a key mediator of the protective effect induced by ischemic preconditioning.
Our data show that CT-1 is a natural defense of the liver against apoptosis. This cytokine may have therapeutic potential.
CT1 decreases cell death through a mechanism related to Stat3 and Akt phosphorylation and activation of calpastatin in D-galactosamine-treated hepatocytes.
The protein encoded by this gene is a secreted cytokine that induces cardiac myocyte hypertrophy in vitro. It has been shown to bind and activate the ILST/gp130 receoptor. Two transcript variants encoding different isoforms have been found for this gene.
, cardiophin 1