ArticleJournal of muscle research and cell motility2012
Adrenergic stress reveals septal hypertrophy and proteasome impairment in heterozygous Mybpc3-targeted knock-in mice.
Article in Journal of muscle research and cell motility, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- An ALPK3 truncation variant causing autosomal dominant hypertrophic cardiomyopathy is partially rescued by mavacamten.Scientific reports · 2025Article
- Zonisamide attenuates pressure overload-induced myocardial hypertrophy in mice through proteasome inhibition.Acta pharmacologica Sinica · 2024Article
- MDM2 Regulation of HIF Signaling Causes Microvascular Dysfunction in Hypertrophic Cardiomyopathy.Circulation · 2023Article
- Western diet triggers cardiac dysfunction in heterozygousJournal of molecular and cellular cardiology plus · 2023Article
- Heterogeneous Distribution of Genetic Mutations in Myosin Binding Protein-C Paralogs.Frontiers in genetics · 2022Article
- NSAIDs-dependent adaption of the mitochondria-proteasome system in immortalized human cardiomyocytes.Scientific reports · 2020Article
- Allelic imbalance and haploinsufficiency in MYBPC3-linked hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019Review
- HspB1 phosphorylation regulates its intramolecular dynamics and mechanosensitive molecular chaperone interaction with filamin C.Science advances · 2019Article
- Article
- Proteasome dysfunction in cardiomyopathies.The Journal of physiology · 2017Review
- Sarcomeric protein modification during adrenergic stress enhances cross-bridge kinetics and cardiac output.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- Review
- A dilated cardiomyopathy mutation blunts adrenergic response and induces contractile dysfunction under chronic angiotensin II stress.American journal of physiology. Heart and circulatory physiology · 2015Article
- I-1-deficiency negatively impacts survival in a cardiomyopathy mouse model.International journal of cardiology. Heart & vasculature · 2015Article
- Research priorities in sarcomeric cardiomyopathies.Cardiovascular research · 2015Review
- Animal and in silico models for the study of sarcomeric cardiomyopathies.Cardiovascular research · 2015Review
- Sarcomere mutation-specific expression patterns in human hypertrophic cardiomyopathy.Circulation. Cardiovascular genetics · 2014Article
- Rare variants in genes encoding MuRF1 and MuRF2 are modifiers of hypertrophic cardiomyopathy.International journal of molecular sciences · 2014Article
- Contractile dysfunction in a mouse model expressing a heterozygous MYBPC3 mutation associated with hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2014Article
- MYBPC3 in hypertrophic cardiomyopathy: from mutation identification to RNA-based correction.Pflugers Archiv : European journal of physiology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy (HCM) is characterized by asymmetric septal hypertrophy and is often caused by mutations in MYBPC3 gene encoding cardiac myosin-binding protein C. In contrast to humans, who are already affected at the heterozygous state, mouse models develop the phenotype mainly at the homozygous state. Evidence from cell culture work suggested that altered proteasome function contributes to the pathogenesis of HCM. Here we tested in two heterozygous Mybpc3-targeted mouse models whether adrenergic stress unmasks a specific cardiac phenotype and proteasome dysfunction. The first model carries a human Mybpc3 mutation (Het-KI), the second is a heterozygous Mybpc3 knock-out (Het-KO). Both models were compared to wild-type (WT) mice. Mice were treated with a combination of isoprenaline and phenylephrine (ISO/PE) or NaCl for 1 week. Whereas ISO/PE induced left ventricular hypertrophy (LVH) with increased posterior wall thickness to a similar extent in all groups, it increased septum thickness only in Het-KI and Het-KO. ISO/PE did not affect the proteasomal chymotrypsin-like activity or β5-subunit protein level in Het-KO or wild-type mice (WT). In contrast, both parameters were markedly lower in Het-KI and negatively correlated with the degree of LVH in Het-KI only. In conclusion, adrenergic stress revealed septal hypertrophy in both heterozygous mouse models of HCM, but proteasome dysfunction only in Het-KI mice, which carry a mutant allele and closely mimic human HCM. This supports the hypothesis that proteasome impairment contributes to the pathophysiology of HCM.
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Registered trials
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