ArticlePloS one2010
Common microRNA signatures in cardiac hypertrophic and atrophic remodeling induced by changes in hemodynamic load.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 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
18 citing papers in PubMed, 33 citations in OpenAlex.
- A Noninvasive Circulating Signature of Combined Right Ventricular Pressure and Volume Overload in Tetralogy of Fallot/Pulmonary Atresia/Major Aortopulmonary Collateral Arteries.World journal for pediatric & congenital heart surgery · 2024Article
- Ventricular unloading causes prolongation of the QT interval and induces ventricular arrhythmias in rat hearts.Frontiers in physiology · 2024Article
- Rapid Pacing Decreases L-type CaThe Journal of membrane biology · 2023Article
- Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype?Biomedicines · 2022Review
- Regulation of microRNA-221, -222, -21 and -27 in articular cartilage subjected to abnormal compressive forces.The Journal of physiology · 2021Article
- The Effects of Regular Exercise on Circulating Cardiovascular-related MicroRNAs.Scientific reports · 2019Article
- Differential MicroRNA expression following head-down tilt bed rest: implications for cardiovascular responses to microgravity.Physiological reports · 2019Article
- Non-coding RNAs in cardiovascular diseases: diagnostic and therapeutic perspectives.European heart journal · 2018Review
- Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation.Bioscience reports · 2018Article
- Identification of miR-34 regulatory networks in settings of disease and antimiR-therapy: Implications for treating cardiac pathology and other diseases.RNA biology · 2017Article
- MicroRNA miR-301a is a novel cardiac regulator of Cofilin-2.PloS one · 2017Article
- Article
- Molecular Mechanisms of Right Ventricular Failure.Circulation · 2015Review
- The vulnerable right ventricle.Current opinion in pediatrics · 2015Review
- Enhanced Ca²+ influx through cardiac L-type Ca²+ channels maintains the systolic Ca²+ transient in early cardiac atrophy induced by mechanical unloading.Pflugers Archiv : European journal of physiology · 2013Article
- miR-222 contributes to sex-dimorphic cardiac eNOS expression via ets-1.Physiological genomics · 2013Article
- Dynamic microRNA expression during the transition from right ventricular hypertrophy to failure.Physiological genomics · 2012Article
- Taking pressure off the heart: the ins and outs of atrophic remodelling.Cardiovascular research · 2011Review
Corrections and comments
- Erratum issuedEmmons, Julius [corrected to Emons, Julius]
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMechanical overload leads to cardiac hypertrophy and mechanical unloading to cardiac atrophy. Both conditions produce similar transcriptional changes including a re-expression of fetal genes, despite obvious differences in phenotype. MicroRNAs (miRNAs) are discussed as superordinate regulators of global gene networks acting mainly at the translational level. Here, we hypothesized that defined sets of miRNAs may determine the direction of cardiomyocyte plasticity responses. METHODOLOGY/PRINCIPAL
findingsWe employed ascending aortic stenosis (AS) and heterotopic heart transplantation (HTX) in syngenic Lewis rats to induce mechanical overloading and unloading, respectively. Heart weight was 26±3% higher in AS (n = 7) and 33±2% lower in HTX (n = 7) as compared to sham-operated (n = 6) and healthy controls (n = 7). Small RNAs were enriched from the left ventricles and subjected to quantitative stem-loop specific RT-PCR targeting a panel of 351 miRNAs. In total, 153 miRNAs could be unambiguously detected. Out of 72 miRNAs previously implicated in the cardiovascular system, 40 miRNAs were regulated in AS and/or HTX. Overall, HTX displayed a slightly broader activation pattern for moderately regulated miRNAs. Surprisingly, however, the regulation of individual miRNA expression was strikingly similar in direction and amplitude in AS and HTX with no miRNA being regulated in opposite direction. In contrast, fetal hearts from Lewis rats at embryonic day 18 exhibited an entirely different miRNA expression pattern.
conclusionsTaken together, our findings demonstrate that opposite changes in cardiac workload induce a common miRNA expression pattern which is markedly different from the fetal miRNA expression pattern. The direction of postnatal adaptive cardiac growth does, therefore, not appear to be determined at the level of single miRNAs or a specific set of miRNAs. Moreover, miRNAs themselves are not reprogrammed to a fetal program in response to changes in hemodynamic load.
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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.