ArticleEuropean journal of heart failure2016
Molecular and structural transition mechanisms in long-term volume overload.
Article in European journal of heart failure, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 64 citations in OpenAlex.
- MMP-9 Gene Ablation Preserves Ejection Fraction During "Single-Hit" Model of HFrEF.Biochemical genetics · 2026Article
- Estimated plasma volume status and the risk of 30-day mortality among patients with traumatic brain injury: analysis from the MIMIC-IV database.Frontiers in neurology · 2026Article
- Contributions of mechanical loading and hormonal changes to eccentric hypertrophy during volume overload: A Bayesian analysis using logic-based network models.PLoS computational biology · 2025Article
- A Need to Preserve Ejection Fraction during Heart Failure.International journal of molecular sciences · 2024Review
- Abnormal phosphorylation / dephosphorylation and CaHeart failure reviews · 2024Review
- Article
- Cerium oxide nanoparticles-carrying human umbilical cord mesenchymal stem cells counteract oxidative damage and facilitate tendon regeneration.Journal of nanobiotechnology · 2023Article
- DNA Methylation Analysis Identifies Novel Epigenetic Loci in Dilated Murine Heart upon Exposure to Volume Overload.International journal of molecular sciences · 2023Article
- Signaling network model of cardiomyocyte morphological changes in familial cardiomyopathy.Journal of molecular and cellular cardiology · 2023Article
- Transcriptomics reveal stretched human pluripotent stem cell-derived cardiomyocytes as an advantageous hypertrophy model.Journal of molecular and cellular cardiology plus · 2022Article
- Hemodynamic stress-induced cardiac remodelling is not modulated by ablation of phosphodiesterase 4D interacting protein.Journal of cellular and molecular medicine · 2022Article
- Different activation of MAPKs and Akt/GSK3β after preload vs. afterload elevation.ESC heart failure · 2022Article
- Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification.Frontiers in cell and developmental biology · 2022Review
- Prognostic significance of liver stiffness assessed by fibrosis-4 index in patients with heart failure.ESC heart failure · 2021Article
- Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling.Scientific reports · 2021Article
- Ultrastructural Adaptation of the Cardiomyocyte to Chronic Mitral Regurgitation.Frontiers in cardiovascular medicine · 2021Article
- NADPH oxidase-4 promotes eccentric cardiac hypertrophy in response to volume overload.Cardiovascular research · 2021Article
- Volume Load-Induced Right Ventricular Failure in Rats Is Not Associated With Myocardial Fibrosis.Frontiers in physiology · 2021Article
- Intrarenal Doppler ultrasonography reflects hemodynamics and predicts prognosis in patients with heart failure.Scientific reports · 2020Observational
- Regulation of titin-based cardiac stiffness by unfolded domain oxidation (UnDOx).Proceedings of the National Academy of Sciences of the United States of America · 2020Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimWe have previously reported that early phase (1 week) of experimental volume overload (VO) has an adaptive phenotype while wall stress-matched pressure overload (PO) is maladaptive. Here we investigate the transition from adaptation to heart failure (HF) in long-term VO. METHODS AND
resultsFVB/N wild-type mice were subjected to VO induced by aortocaval shunt, and were followed by serial echocardiography until in vivo left ventricular ejection fraction was below <50% (135 ± 35 days). Heart failure was evident from increased lung and liver weight and increased mortality compared with sham. Maladaptive remodelling resulted in significantly reduced sarcomeric titin phosphorylation (causing increased sarcomeric stiffness), whereas interstitial fibrosis was not increased. This was paralleled by re-expression of the fetal gene program, activation of calcium/calmodulin-dependent protein kinase II (CaMKII), decreased protein kinase B (Akt) phosphorylation, high oxidative stress, and increased apoptosis. Consistently, development of HF and mortality were significantly aggravated in Akt-deficient mice.
conclusionTransition to HF in VO is associated with decreased Akt and increased CaMKII signalling pathways together with increased oxidative stress and apoptosis. Lack of interstitial fibrosis together with sarcomeric titin hypophosphorylation indicates an increased stiffness at the sarcomeric but not matrix level in VO-induced HF (in contrast to PO). Transition to HF may result from myocyte loss and myocyte dysfunction owing to increased stiffness.
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