ReviewCardiovascular research2011
Taking pressure off the heart: the ins and outs of atrophic remodelling.
Review in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 59 citations in OpenAlex.
- Exercise-induced cardiac hypertrophy: cellular and molecular mechanisms of cardiac adaptation following physical activity.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2026Review
- Prospective evaluation of speckle-tracking echocardiography for detecting functionally significant coronary artery disease: a quantitative flow ratio-based study.Quantitative imaging in medicine and surgery · 2026Article
- Article
- Beyond the right ventricle: assessment of the left ventricular function in pulmonary hypertension.Frontiers in medicine · 2026Review
- A New Semi-Quantitative Parameter to Assess Functionally Significant Coronary Disease Using Myocardial Contrast Echocardiography.Reviews in cardiovascular medicine · 2024Article
- Central Actions of Leptin Induce an Atrophic Pattern and Improves Heart Function in Lean Normoleptinemic Rats via PPARβ/δ Activation.Biomolecules · 2024Article
- Autophagy and ubiquitin-dependent proteolysis processes in left ventricular mass loss in pulmonary arterial hypertension.Scientific reports · 2024Article
- Molecular Pathways and Animal Models of Cardiomyopathies.Advances in experimental medicine and biology · 2024Article
- Cardiomyocyte external mechanical unloading activates modifications of α-actinin differently from sarcomere-originated unloading.The FEBS journal · 2023Article
- Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype?Biomedicines · 2022Review
- Susceptibility of female rats to cardiac arrhythmias following refeeding after severe food restriction.Biology of sex differences · 2022Article
- Short-Chain Fatty Acids in the Metabolism of Heart Failure - Rethinking the Fat Stigma.Frontiers in cardiovascular medicine · 2022Review
- Cardio-sarcopenia: A syndrome of concern in aging.Frontiers in medicine · 2022Article
- Lower Cardiorespiratory Fitness Is Associated With Right Ventricular Geometry and Function - The Sedentary's Heart: SHIP.Journal of the American Heart Association · 2021Article
- Thbs1 induces lethal cardiac atrophy through PERK-ATF4 regulated autophagy.Nature communications · 2021Article
- Knockout of MYOM1 in human cardiomyocytes leads to myocardial atrophy via impairing calcium homeostasis.Journal of cellular and molecular medicine · 2021Article
- Heart Failure Syndrome With Preserved Ejection Fraction Is a Metabolic Cluster of Non-resolving Inflammation in Obesity.Frontiers in cardiovascular medicine · 2021Review
- Myocardial proteomic profile in pulmonary arterial hypertension.Scientific reports · 2020Article
- Changes in heart morphometric parameters over the course of a monocrotaline-induced pulmonary arterial hypertension rat model.Journal of translational medicine · 2020Article
- Alteration of calcium signalling in cardiomyocyte induced by simulated microgravity and hypergravity.Cell proliferation · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Our work on atrophic remodelling of the heart has led us to appreciate the simple principles in biology: (i) the dynamic nature of intracellular protein turnover, (ii) the return to the foetal gene programme when the heart remodels, and (iii) the adaptive changes of cardiac metabolism. Although the molecular mechanisms of cardiac hypertrophy are many, much less is known regarding the molecular mechanisms of cardiac atrophy. We state the case that knowing more about mechanisms of atrophic remodelling may provide insights into cellular consequences of metabolic and haemodynamic unloading of the stressed heart. Overall we strive to find an answer to the question: 'What makes the failing heart shrink and become stronger?' We speculate that signals arising from intermediary metabolism of energy-providing substrates are likely candidates.
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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.