ArticleTransgenic research2012
Cardioprotection by Hepc1 in cTnT(R141W) transgenic mice.
Article in Transgenic research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- The prognostic value of serum hepcidin-25 in predicting cardiovascular events among maintenance hemodialysis patients: insights from the INFINITY cohort.Clinical and experimental nephrology · 2025Observational
- Cardiomyocyte-specific overexpression of FPN1 diminishes cardiac hypertrophy induced by chronic intermittent hypoxia.Journal of cellular and molecular medicine · 2024Article
- Long noncoding RNA AVAN promotes antiviral innate immunity by interacting with TRIM25 and enhancing the transcription of FOXO3a.Cell death and differentiation · 2021Article
- Iron Absorption in Celiac Disease and Nutraceutical Effect of 7-Hydroxymatairesinol. Mini-Review.Molecules (Basel, Switzerland) · 2020Review
- New Insights into the Hepcidin-Ferroportin Axis and Iron Homeostasis in iPSC-Derived Cardiomyocytes from Friedreich's Ataxia Patient.Oxidative medicine and cellular longevity · 2019Article
- Balance of cardiac and systemic hepcidin and its role in heart physiology and pathology.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Article
- Gene-Targeted Mice with the Human Troponin T R141W Mutation Develop Dilated Cardiomyopathy with Calcium Desensitization.PloS one · 2016Article
- The functional effect of dilated cardiomyopathy mutation (R144W) in mouse cardiac troponin T is differently affected by α- and β-myosin heavy chain isoforms.American journal of physiology. Heart and circulatory physiology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepcidin 1 (Hepc1) is a peptide hormone secreted by the liver in response to iron loading. It is expressed in the heart and is thought to play a role in the regulation of iron homeostasis in an autocrine and paracrine fashion. We have shown that expression of Hepc1 is strongly down-regulated in the heart of the cTnT(R141W) transgenic mouse model of dilated cardiomyopathy (DCM) at 3 months of age. Transgenic mice with heart tissue-specific Hepc1 expression alone or in combination with the cTnT(R141W) mutation were produced to study the effects of Hepc1 on DCM. Transgenic expression of Hepc1 was found to be nonlethal and resulted in decreased mortality in cTnT(R141W) transgenic mice, from 29.6 to 7.4%(n = 27; P < 0.05), through 7 months of age. Expression of Hepc1 also brought about increases in the left ventricular wall, as well as ejection fraction and fractional shortening. In addition, the expression of Hepc1 inhibited the fibrosis and ultra-structural alterations seen in cTnT(R141W) transgenic mice. Furthermore, transgenic expression of Hepc1 restored the iron level and phosphorylation level of extracellular signal-regulated kinases 1/2 (ERK1/2) in the heart tissues of cTnT(R141W) transgenic mice. It was concluded that transgenic expression of Hepc1 compensated for the loss of Hepc1 expression and the release of iron and brought about a marked improvement in the pathologic phenotype of DCM, in which the ERK1/2 signal pathway might play an important role.
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