ArticleJournal of molecular and cellular cardiology2010
Attenuated hypertrophic response to pressure overload in a lamin A/C haploinsufficiency mouse.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 65 citations in OpenAlex.
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
- Myonuclear alterations associated with exercise are independent of age in humans.The Journal of physiology · 2025Article
- Non-Cell-Autonomous Cardiomyocyte Regulation Complicates Gene Supplementation Therapy forJACC. Basic to translational science · 2024Article
- Nucleus Mechanosensing in Cardiomyocytes.International journal of molecular sciences · 2023Review
- A Multisensory Network Drives Nuclear Mechanoadaptation.Biomolecules · 2022Review
- Viscoelasticity, Like Forces, Plays a Role in Mechanotransduction.Frontiers in cell and developmental biology · 2022Review
- Intermediate filaments: Integration of cell mechanical properties during migration.Frontiers in cell and developmental biology · 2022Review
- Gpx3 and Egr1 Are Involved in Regulating the Differentiation Fate of Cardiac Fibroblasts under Pressure Overload.Oxidative medicine and cellular longevity · 2022Article
- Pathogenic Mechanisms of Hypertrophic Cardiomyopathy beyond Sarcomere Dysfunction.International journal of molecular sciences · 2021Review
- The nuclear envelope: LINCing tissue mechanics to genome regulation in cardiac and skeletal muscle.Biology letters · 2020Article
- Force-induced gene up-regulation does not follow the weak power law but depends on H3K9 demethylation.Science advances · 2020Article
- The Broad Spectrum ofFrontiers in physiology · 2020Review
- Adjustable viscoelasticity allows for efficient collective cell migration.Seminars in cell & developmental biology · 2019Review
- Mechanical regulation of gene expression in cardiac myocytes and fibroblasts.Nature reviews. Cardiology · 2019Review
- Deformation Microscopy for Dynamic Intracellular and Intranuclear Mapping of Mechanics with High Spatiotemporal Resolution.Cell reports · 2019Article
- Signal Transduction across the Nuclear Envelope: Role of the LINC Complex in Bidirectional Signaling.Cells · 2019Review
- Single Cell Imaging of Nuclear Architecture Changes.Frontiers in cell and developmental biology · 2019Article
- Linker of nucleoskeleton and cytoskeleton complex proteins in cardiomyopathy.Biophysical reviews · 2018Review
- Emerging views of the nucleus as a cellular mechanosensor.Nature cell biology · 2018Review
- Luma is not essential for murine cardiac development and function.Cardiovascular research · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Inherited mutations cause approximately 30% of all dilated cardiomyopathy cases, with autosomal dominant mutations in the LMNA gene accounting for more than one third of these. The LMNA gene encodes the nuclear envelope proteins lamins A and C, which provide structural support to the nucleus and also play critical roles in transcriptional regulation. Functional deletion of a single allele is sufficient to trigger dilated cardiomyopathy in humans and mice. However, whereas Lmna(-/-) mice develop severe muscular dystrophy and dilated cardiomyopathy and die by 8 weeks of age, heterozygous Lmna(+/-) mice have a much milder phenotype, with changes in ventricular function and morphology only becoming apparent at 1 year of age. Here, we studied 8- to 20-week-old Lmna(+/-) mice and wild-type littermates in a pressure overload model to examine whether increased mechanical load can accelerate or exacerbate myocardial dysfunction in the heterozygotes. While overall survival was similar between genotypes, Lmna(+/-) animals had a significantly attenuated hypertrophic response to pressure overload as evidenced by reduced ventricular mass and myocyte size. Analysis of pressure overload-induced transcriptional changes suggested that the reduced hypertrophy in the Lmna(+/-) mice was accompanied by impaired activation of the mechanosensitive gene Egr-1. In conclusion, our findings provide further support for a critical role of lamins A and C in regulating the cellular response to mechanical stress in cardiomyocytes and demonstrate that haploinsufficiency of lamins A and C alone is sufficient to alter hypertrophic responses and cardiac function in the face of pressure overload in the heart.
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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.