ArticleCytokine2006
The lack of cardiotrophin-1 alters expression of interleukin-6 and leukemia inhibitory factor mRNA but does not impair cardiac injury response.
Article in Cytokine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Molecular and cellular neurocardiology in heart disease.The Journal of physiology · 2025Review
- Role of Circulating Biomarkers in Diabetic Cardiomyopathy.Biomedicines · 2024Review
- Ischemia-reperfusion myocardial infarction induces remodeling of left cardiac-projecting stellate ganglia neurons.American journal of physiology. Heart and circulatory physiology · 2024Article
- Role of novel biomarkers in diabetic cardiomyopathy.World journal of diabetes · 2021Review
- Molecular and cellular neurocardiology: development, and cellular and molecular adaptations to heart disease.The Journal of physiology · 2016Review
- Myocardial Infarction Causes Transient Cholinergic Transdifferentiation of Cardiac Sympathetic Nerves via gp130.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Neuropathies of Stüve-Wiedemann Syndrome due to mutations in leukemia inhibitory factor receptor (LIFR) gene.Journal of neurology & neuromedicine · 2016Article
- Stüve-Wiedemann syndrome: LIFR and associated cytokines in clinical course and etiology.Orphanet journal of rare diseases · 2014Review
- Depletion of cellular glutathione modulates LIF-induced JAK1-STAT3 signaling in cardiac myocytes.The international journal of biochemistry & cell biology · 2012Article
- Cardiac ischemia-reperfusion regulates sympathetic neuropeptide expression through gp130-dependent and independent mechanisms.Neuropeptides · 2011Article
- Infarction-induced cytokines cause local depletion of tyrosine hydroxylase in cardiac sympathetic nerves.Experimental physiology · 2010Article
- Absence of gp130 in dopamine beta-hydroxylase-expressing neurons leads to autonomic imbalance and increased reperfusion arrhythmias.American journal of physiology. Heart and circulatory physiology · 2009Article
- The immune system and cardiac repair.Pharmacological research · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiotrophin-1 (CT-1) was identified as a growth factor for cardiac myocytes and CT-1 protects myocytes from cell death. Adult CT-1(-/-) mice exhibit neural deficits including the loss of preganglionic sympathetic neurons, but their autonomic and cardiac parameters have not been examined. We used these mice to determine if the absence of CT-1 or loss of preganglionic sympathetic input altered heart rate, left ventricular pressure, cardiac contractility (dP/dt), or cell death following ischemia-reperfusion. Basal heart rate was increased in CT-1(-/-) mice, and this difference was abolished by ganglionic block. Left ventricular pressure and dP/dt were unchanged. Dobutamine stimulated similar increases in heart rate and dP/dt in both genotypes, but ventricular pressure was significantly lower in CT-1 nulls. Cardiac expression of interleukin-6 (IL-6) mRNA was increased significantly in CT-1 null mice, while leukemia inhibitory factor (LIF) mRNA was unchanged. Infarct size normalized to area at risk was no different in CT-1(-/-) mice (33.8+/-1.0% vs. 37.7+/-3.2% WT) 24h after ischemia-reperfusion. Induction of IL-6 mRNA after infarct was significantly abrogated in CT-1 null mice compared to wild-type mice, but LIF mRNA-induction remained significant in CT-1 null mice and might contribute to cardiac protection in the absence of CT-1.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.